ICML 2026 论文列表

As the demand for emotional intelligence in large language models (LLMs) grows, a key challenge lies in understanding the internal mechanisms that give rise to emotional expression and in controlling emotions in generated text. This study addresses three core questions: (1) Do LLMs contain context-agnostic mechanisms shaping emotional expression? (2) What form do these mechanisms take? (3) Can they be harnessed for universal emotion control? We first construct a controlled dataset, $\textit{SEV}$ (Scenario–Event with Valence), to elicit comparable internal states across emotions. Subsequently, we extract context-agnostic emotion directions that reveal consistent, cross-context encoding of emotion (Q1). We identify neurons and attention heads that locally implement emotional computation through analytical decomposition and causal analysis, and validate their causal roles via ablation and enhancement interventions. Next, we quantify each sublayer's causal influence on the model’s final emotion representation and integrate the identified local components into coherent global emotion circuits that drive emotional expression (Q2). Directly modulating these circuits achieves 99.65% emotion-expression accuracy on the test set, surpassing prompting- and steering-based methods (Q3). To our knowledge, this is the first systematic study to uncover and validate emotion circuits in LLMs, offering new insights into interpretability and controllable emotional intelligence.

We propose causal preference elicitation, a Bayesian framework for expert-in-the-loop causal discovery that actively queries local edge relations to concentrate a posterior over directed acyclic graphs (DAGs). From any black-box observational posterior, we model noisy expert judgments with a three-way likelihood over edge existence and direction. Posterior inference uses a flexible particle approximation, and queries are selected by an efficient expected information gain criterion on the expert’s categorical response. Experiments on synthetic graphs, protein signaling data, and a human gene perturbation benchmark show faster posterior concentration and improved recovery of directed effects under tight query budgets.

Most causal discovery methods recover a completed partially directed acyclic graph (CPDAG) representing a Markov equivalence class from observational data. Recent work has extended these methods to federated settings to address data decentralization and privacy constraints, but often under idealized assumptions that all clients share the same causal model. Such assumptions are unrealistic in practice, as client-specific policies, for instance, across hospitals, naturally induce heterogeneous and unknown interventions. In this work, we address federated causal discovery under unknown client-level interventions. We propose I-PERI, a novel federated algorithm that first recovers the CPDAG common to all clients and then orients additional edges by exploiting structural differences induced by interventions across clients. This yields a tighter equivalence class, which we call the $\mathbf{\Phi}$-Markov Equivalence Class, represented by an augmented version of the CPDAG, namely, a $\mathbf{\Phi}$-CPDAG. We provide theoretical guarantees on the convergence of I-PERI, as well as on its privacy-preserving properties, and present empirical evaluations demonstrating the effectiveness of the proposed algorithm.

The performance of sparse direct solvers is fundamentally governed by fill-in, i.e. new nonzero entries arising from the LU factorization of a sparse matrix, as they dictate memory footprint and subsequent computation time. For decades, a variety of graph-theoretic algorithms have aimed to minimize fill-in, a problem known to be both NP-hard and critically important. While recent deep learning methods, optimizing surrogate fill-in objectives, show empirical promise and can outperform classical algorithms on certain matrices, they offer limited interpretability into the underlying mechanism of fill-in generation. To address this, we propose a novel reordering approach, Causal Triplet Structure Learning (CTS), which is grounded in the Fill-Path Theorem and reduces arbitrary-length fill-paths to length-two candidate triplets, identifies the causal structures that trigger fill-in, and intervenes to block their formation. Empirically, we design a multigrid-style GAT with KAN activations to learn vertex embeddings and introduce a causal triplet loss that discourages such structures during training. Experiments on the SuiteSparse Matrix Collection demonstrate that our method reduces fill-in by 6$\times$, leading to 12$\times$ speedup in factorization time compared to state-of-the-art methods on Chemical Process Simulation and Computational Fluid Dynamics matrices.

The problem of domain generalization concerns learning predictive models that are robust to distribution shifts when deployed in new, previously unseen environments. Existing methods typically require labeled data from multiple training environments, limiting their applicability when labeled data are scarce. In this work, we study domain generalization in an anti-causal setting, where the outcome causes the observed covariates. Under this structure, environment perturbations that affect the covariates do not propagate to the outcome, which motivates regularizing the model's sensitivity to these perturbations. Crucially, estimating these perturbation directions does not require labels, enabling us to leverage unlabeled data from multiple environments. We propose two methods that penalize the model's sensitivity to variations in the mean and covariance of the covariates across environments, respectively, and prove that these methods have worst-case optimality guarantees under certain classes of environments. Finally, we demonstrate the empirical performance of our approach on a controlled physical system and a physiological signal dataset.

Causal discovery is essential for advancing data-driven fields such as scientific AI and data analysis, yet existing approaches face significant time- and space-efficiency bottlenecks when scaling to large graphs. To address this challenge, we present CauScale, a neural architecture designed for efficient causal discovery that scales inference to graphs with up to 1000 nodes. CauScale improves time efficiency via a reduction unit that compresses data embeddings and improves space efficiency by adopting tied attention weights to avoid maintaining axis-specific attention maps. To keep high causal discovery accuracy, CauScale adopts a two-stream design: a data stream extracts relational evidence from high-dimensional observations, while a graph stream integrates statistical graph priors and preserves key structural signals. CauScale successfully scales to 500-node graphs during training, where prior work fails due to space limitations. Across testing data with varying graph scales and causal mechanisms, CauScale achieves 99.6\% mAP on in-distribution data and 84.4\% on out-of-distribution data, while delivering 4$\times$–13,000$\times$ inference speedups over prior methods.

The scalability of Large Language Models to long sequences is hindered by the quadratic cost of self-attention and the limitations of positional encodings. To address these, we introduce **Caracal**, a novel architecture that replaces self-attention with a parameter-efficient, $\mathcal{O}(L \log L)$ Multi-Head Fourier (MHF) module. Our contributions are threefold: (1) We leverage the Fast Fourier Transform (FFT) for sequence mixing, inherently addressing both bottlenecks mentioned above. (2) We apply a frequency-domain causal masking technique that enforces autoregressive capabilities via asymmetric padding and truncation, overcoming a critical barrier for Fourier-based generative models. (3) Unlike efficient models relying on hardware-specific implementations (e.g., Mamba), **Caracal** uses standard library operators. This ensures robust portability, eliminating common deployment barriers. Evaluations demonstrate that **Caracal** performs competitively with Transformer and SSM baselines, offering a scalable and simple pathway for efficient long-sequence modeling. Code is available in the supplementary materials.

Building on recent formalizations of root cause analysis for rare events (“outliers”) in structural equation models, we propose a formal definition of a causal pathway and discuss its testable implications. We identify conditions under which these implications depend only on a causal abstraction defined by the pathway of rare events, rather than on the full causal graph of the underlying system. Accordingly, we introduce an abstraction of causal structure to pathways of rare events that bridges simple verbal causal explanations and detailed causal modeling.

Disentangled representation learning is a powerful paradigm for robust attribute prediction. While recent methods address attribute correlations, hidden correlations remain underexplored, where data under the value of a certain attribute exhibit underlying modes correlated with other attributes. To preserve mode information and achieve disentanglement, we jointly discover modes and enforce mode-based conditional independence. Yet, the interdependency between these two modules may lead to error amplification under naive iterations. We propose Coordinated Disentanglement with Iterative mode Discovery (CoDID), an end-to-end framework featuring a dynamic architecture that adapts to evolving number of modes, and a coordination mechanism that mitigates error amplification via meta-optimization. Empirical results demonstrate the state-of-the-art performance on diverse tasks.

Classical sample complexity bounds for causal structure learning are minimax in nature, characterizing worst-case difficulty without distinguishing between easy and hard instances. We study instance-specific complexity for Markov equivalence class (MEC) recovery in linear Gaussian structural equation models. We introduce the Fisher dimension, defined as the inverse squared minimum partial correlation that must be detected to recover the MEC. We prove that the Fisher dimension governs sample complexity: it provides both a lower bound and an upper bound (tight up to logarithmic factors) for MEC recovery. A key theoretical finding is that under spectrally well-conditioned models, with bounded noise variances, bounded covariance eigenvalues, and constant-order edge coefficients, the Fisher dimension is uniformly bounded regardless of graph structure. Thus, significant instance-specific variation arises from parametric rather than structural features. Empirical validation shows strong correlation between our predictor and observed sample complexity for structured graph families.

Differentiable approaches to causal discovery have shown promise in learning DAG structures via continuous optimization, but their theoretical guarantees are largely restricted to models with homoscedastic noise or known noise distribution. In particular, existing methods based on mean squared error fail to identify the true DAG when noise distributions are non-Gaussian and vary in scale. In this paper, we address this gap in nonlinear additive noise models (ANMs) with arbitrary noise. Our approach extends NOTIME (Berrevoets et al. 2025) which minimizes an independence criterion among the residuals. We show that the global minimizer of the independence criterion corresponds to the true underlying DAG up to additional constant edges in general ANMs. To recover the exact structure, we introduce an adaptive group lasso penalty that regularizes entire columns of the first-layer weight matrix of an MLP, enabling the selective pruning of constant edges in a functionally meaningful way. Empirically, our method achieves effective and stable performance across diverse noise types and variances, outperforming prior methods that lack identifiability guarantees in this setting.

Adapting to latent confounded shift remains a core challenge in modern AI. This setting is driven by hidden variables that induce spurious correlations between inputs and outputs during training, leading models to rely on non-causal shortcuts. For example, a model may learn to treat metadata (e.g., data source like "Amazon") as a proxy for positive sentiment, causing failure when the source becomes predominantly negative during deployment. To address this *latent confounded shift*, we introduce Causal Fine-Tuning (CFT). Using a structural causal model as an inductive bias, we derive sufficient identification conditions that motivate a fine-tuning objective for decomposing representations into high-level stable and low-level shift-sensitive components. Instantiating this framework in BERT, we show that learning such causal/spurious representations and adjusting them accordingly yield a more robust predictor. Experiments on spurious correlation injection attacks in text demonstrate that our method outperforms black-box domain generalization baselines, highlighting the benefits of explicitly modeling causal structure.

Model-Based Reinforcement Learning yields sample efficiency via latent imagination, yet remains constrained by **Historical Tethering**: imagination is typically initialized from observed states. This creates a learning asymmetry, where the world model's manifold discovery outpaces the policy's sparse-reward optimization. We propose **Mind Dreamer (MD)**, a framework that instantiates **Active Causal Intervention** to transcend Markovian continuity. MD reformulates discovery as the minimization of a global Relay Expected Free Energy. Instead of initializing from historical data, it draws initial states from an adversarial generator $s_0 \sim p_{gen}(\cdot)$, creating non-continuous **latent jumps** to epistemic blind spots that are physically plausible yet cognitively challenging. We derive **Relay Value Function** and **Relay Uncertainty Function** to resolve the credit assignment paradox across these spatial ruptures. Treating synthesized anchors as interventional intermediary states, these potentials propagate pragmatic and epistemic value through Bellman-style backups. Notably, we prove that uncertainty propagation across discontinuities necessitates a quadratic discount $\gamma^2$, establishing a formal epistemic horizon. Theoretically, MD approximates a variance-minimizing importance sampler that expands the manifold's spectral gap, reducing the hitting time to critical bottleneck states. Empirically, MD achieves a **1.67$\times$ average speedup** over DreamerV3 on DeepMind Control Suite, reaching **8.8$\times$** in sparse-reward tasks.

Understanding climate dynamics requires going beyond correlations in observational data to uncover their underlying causal process. Latent drivers, such as atmospheric processes, play a critical role in temporal dynamics, while direct causal influences also exist among geographically proximate observed variables. Traditional Causal Representation Learning (CRL) typically focuses on latent factors but overlooks such observable-to-observable causal relations, limiting its applicability to climate analysis. In this paper, we introduce a unified framework that jointly uncovers (i) causal relations among observed variables and (ii) latent driving forces together with their interactions. We establish conditions under which both the hidden dynamic processes and the causal structure among observed variables are simultaneously identifiable from time-series data. Remarkably, our guarantees hold even in the nonparametric setting, leveraging contextual information to recover latent variables and observable relations. Building on these insights, we propose CaDRe (Causal Discovery and Representation learning), a time-series generative model with structural constraints that integrates CRL and causal discovery. Experiments on synthetic datasets validate our theoretical results. On real-world climate datasets, CaDRe not only delivers competitive forecasting accuracy but also recovers visualized causal graphs aligned with domain expertise, thereby offering interpretable insights into climate systems.

Estimating treatment effects from observational text is increasingly practical with Large Language Models (LLMs). However, applying causal representation learning directly to high-dimensional LLM embeddings faces a fundamental barrier: empirical Wasserstein matching suffers from the curse of dimensionality, rendering standard generalization guarantees effectively vacuous. We propose SPIKED-CFR, a framework bridging this gap by assuming a Spiked Structure, where treatment selection bias is assumed to manifest primarily as a low-dimensional treated--control discrepancy in the semantic representation. We develop Wasserstein Projection Pursuit, a minimax objective that adversarially learns an orthogonal projection on the Stiefel manifold to identify and balance only this subspace while preserving prognostic information. Under a spiked structure, we show the projected discrepancy can be estimated at a rate governed by the intrinsic dimension $k \ll D$, and we derive a tighter PEHE generalization bound that depends on $k$ rather than the ambient embedding dimension. Experiments on four semi-synthetic benchmarks and four real-world clinical benchmarks demonstrate improved accuracy and robustness over strong baselines.

Causal discovery in time series is increasingly performed using nonlinear machine-learning models, yet the resulting causal relationships are almost always summarized by scalar edge scores. We argue that this practice obscures the true object learned by nonlinear autoregressive models: a state-dependent function whose effect varies across regimes, magnitudes, and contexts. We formalize function-valued causal influence for additive, contribution-decomposable architectures and show that scalar causal scores constitute a severe information bottleneck, conflating between-state variation with within-state residual noise. Using Neural Additive Vector Autoregression as a representative architecture, we introduce a practical framework based on Individual Conditional Expectation for estimating causal response functions directly from trained models. Through controlled synthetic experiments, we demonstrate that edges with indistinguishable scalar scores can exhibit qualitatively different functional behaviors, including monotonic, thresholded, saturating, and sign-changing effects. An applied case study on democratic development further shows that function-valued analysis reveals regime-specific and asymmetric causal structure systematically missed by score-centric approaches.

Supervised Causal Learning has shown promise in causal discovery, yet it often struggles with generalization across diverse interventional settings, particularly when intervention targets are unknown. To address this, we propose TICL (Test-time Interventional Causal Learning), a novel method that synergizes Test-Time Training with Joint Causal Inference (JCI). Specifically, we design a self-augmentation strategy to generate instance-specific training data at test time, effectively avoiding distribution shifts. Furthermore, by integrating JCI, we developed a PC-inspired two-phase supervised learning scheme, which effectively leverages self-augmented data while ensuring theoretical identifiability. Extensive experiments on bnlearn benchmarks demonstrate TICL's superiority in multiple aspects of causal discovery and intervention target detection.

The do-calculus defines a general system of inference for interventional queries, allowing causal quantities to be transformed through successive applications of its rules. This process induces a rich space of equivalent interventional expressions, but combining and ordering these rules remains challenging. In this work, we introduce derivation graphs, which represent how do-calculus rules are applied and combined, and characterize the full space of observational and interventional probabilities which are equivalent under the do-calculus. The structure of these graphs yields a simple procedure that uses at most four applications of do-calculus rules. Finally, we show how applying identification algorithms to equivalent causal queries produces multiple valid estimands for the same causal quantity, eventually yielding more efficient estimators.

Estimating causal structure in the presence of latent variables is an important yet challenging problem. Recent works have shown that distributional constraints, such as rank deficiency constraints of the covariance matrices, can be exploited to recover the underlying causal structure involving latent variables. However, real-world data often exhibit heterogeneity/nonstationarity, which pose challenges to existing methods. In this work, we develop a principled approach for identifying the structure of partially observed linear causal models from heterogenous/nonstationary data. We first formulate a class of heterogenous/nonstationary, partially observed linear causal models and prove that their distributional constraints are equivalent to those in the homogeneous case. Building on this, we propose a novel rank deficiency test that can efficiently handle heterogenous/nonstationary data, and further establish identifiability results for recovering the causal structure involving latent variables. We also provide a method to identify which variables exhibit distribution shifts, i.e., whose causal mechanisms vary across domains. Experiments on simulated and real-world data validate our theoretical findings and the effectiveness of our method.