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No Free Checker: A Survey of Verifiers for Robot Policies

arXiv:2609.09250v1 Announce Type: cross Abstract: A verifier for robot policies reads a candidate behavior and returns a score for how well it did, used both to evaluate vision-language-action policies and to train them. Verifiers range from success detectors and reward models to runtime monitors, safety filters, and temporal-logic specifications. We survey roughly 150 verifiers and compare them along two properties. Availability is how much a verdict costs, how early in a rollout the verdict arrives, and how often a verdict can be asked for. Availability rises as verdicts get cheaper, earlier, and denser. Credibility is how much a high score tells us about the task. Credibility falls as the judgment becomes gameable and self-serving. We group the verifiers by who supplies the judgment: human verifiers, rule-based and formal verifiers, learned and pretrained verifiers, and model-intrinsic verifiers. Across the four families, we find that credibility falls as availability rises. Regardless of who supplies the judgment, there is no free checker. We then examine what validates a verifier itself, and how much a high score tells us. Three measures appear in the literature: agreement with human labels, the performance of the policy it trains, and behavior under reward hacking. We close with nine metrics that make a verifier claim checkable, and coordinates for the verifiers still to be built.
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A Taxonomy of Architecture Options for Foundation Model-based Agents: Analysis and Decision Model

arXiv:2408.02920v2 Announce Type: replace-cross Abstract: The rapid advancement of AI technology has led to widespread applications of agent systems across various domains. However, the need for detailed architecture design poses significant challenges in designing and operating these systems. This paper introduces a taxonomy focused on the architectures of foundation-model-based agents, addressing critical aspects such as functional capabilities and non-functional qualities. We also discuss the operations involved in both design-time and run-time phases, providing a comprehensive view of architectural design and operational characteristics. By unifying and detailing these classifications, our taxonomy aims to improve the design of foundation-model-based agents. Additionally, the paper establishes a decision model that guides critical design and runtime decisions, offering a structured approach to enhance the development of foundation-model-based agents. Our contributions include providing a structured architecture design option and guiding the development process of foundation-model-based agents, thereby addressing current fragmentation in the field.
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Bit-Flip Attacks on Vision-Language-Action Models: Action-Decoding Architecture Shapes the Vulnerability

arXiv:2608.15475v3 Announce Type: replace-cross Abstract: Quantized Vision-Language-Action (VLA) models expose a weight-fault surface: Rowhammer-style faults can corrupt deployed INT8 bits. We present the first bit-flip attack on a VLA: a few gradient-selected flips reduce closed-loop success to $0\%$, while hundreds of random flips are harmless. Across four model variants spanning three action-head families, damaging bits concentrate in a few action-generating layers, but the empirical budget depends sharply on the head: direct regression and token policies fall in $1$--$5$ flips, whereas the evaluated flow-matching policies require ${\sim}100$--$300$. Our fixed-direction manifold-escape loss cuts \pizero{}'s budget from ${\sim}1000$ to ${\sim}100$ flips, and a matched five-direction sweep shows that the attack is not specific to an all-positive direction. On a direct head, protecting $3.1\%$ of weights preserves $60\%$ success at $K{=}100$, and protecting $5.3\%$ moves the open-loop break threshold from 3 to 100 flips. Finally, task-calibrated emulated $K{=}100$ flips yield $0/20$ real-robot successes, versus $14/20$ clean and $16/20$ global-random. Weight integrity is therefore a security boundary for embodied foundation models. Code is included as ancillary material.
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A programmed cell death learning signature predicts immunotherapy response and identifies AP1S1 as a regulator of immune exclusion in breast cancer

Chin J Cancer Res. 2026 Aug 30;38(4):480-500. doi: 10.21147/j.issn.1000-9604.2026.04.08.

ABSTRACT

OBJECTIVE: Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in the breast cancer immune microenvironment remains poorly understood.

METHODS: We integrated multi-omics data from six breast cancer cohorts (N=3,764) to develop a programmed cell death learning signature (PCDsig) using over 100 machine learning combinations. The model was benchmarked against 29 published signatures. Single-cell transcriptomic analysis decoded the immune landscape and cellular crosstalk. The role of adaptor-related protein complex 1 subunit sigma 1 (AP1S1) was validated through a clinical cohort, in vitro functional assays, and in vivo syngeneic mouse models.

RESULTS: PCDsig significantly stratified patient prognosis across all cohorts, consistently outperforming 29 existing models. High PCDsig scores correlated with immune-excluded phenotypes, reduced CD8+ T cell infiltration, and lower immunophenoscores. Single-cell analysis revealed that high-PCDsig tumors utilize vascular endothelial growth factor A (VEGFA) signaling to foster an immunosuppressive microenvironment. AP1S1 was identified as the core driver of immune exclusion. And our clinical cohort supported the immune exclusion effect of AP1S1. AP1S1 knockdown impaired tumor progression in vitro and fundamentally remodeled the tumor immune ecosystem in vivo. Combining AP1S1 inhibition with anti-programmed cell death ligand 1 (anti-PD-L1) therapy exerted profound synergistic effects, driven by massive infiltration and functional activation of cytotoxic Granzyme B (GZMB)+CD8+ T cells.

CONCLUSIONS: Our study establishes the PCDsig we developed is a potential prognostic and predictive biomarker for breast cancer. We provide the first evidence of AP1S1 as a core immunomodulatory oncogene that mediates immune exclusion. Targeting AP1S1 represents a highly promising strategy to sensitize cold breast tumors to ICB, offering a new perspective for precision immunotherapy.

PMID:42712842 | PMC:PMC13551362 | DOI:10.21147/j.issn.1000-9604.2026.04.08

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A programmed cell death learning signature predicts immunotherapy response and identifies AP1S1 as a regulator of immune exclusion in breast cancer

Chin J Cancer Res. 2026 Aug 30;38(4):480-500. doi: 10.21147/j.issn.1000-9604.2026.04.08.

ABSTRACT

OBJECTIVE: Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in the breast cancer immune microenvironment remains poorly understood.

METHODS: We integrated multi-omics data from six breast cancer cohorts (N=3,764) to develop a programmed cell death learning signature (PCDsig) using over 100 machine learning combinations. The model was benchmarked against 29 published signatures. Single-cell transcriptomic analysis decoded the immune landscape and cellular crosstalk. The role of adaptor-related protein complex 1 subunit sigma 1 (AP1S1) was validated through a clinical cohort, in vitro functional assays, and in vivo syngeneic mouse models.

RESULTS: PCDsig significantly stratified patient prognosis across all cohorts, consistently outperforming 29 existing models. High PCDsig scores correlated with immune-excluded phenotypes, reduced CD8+ T cell infiltration, and lower immunophenoscores. Single-cell analysis revealed that high-PCDsig tumors utilize vascular endothelial growth factor A (VEGFA) signaling to foster an immunosuppressive microenvironment. AP1S1 was identified as the core driver of immune exclusion. And our clinical cohort supported the immune exclusion effect of AP1S1. AP1S1 knockdown impaired tumor progression in vitro and fundamentally remodeled the tumor immune ecosystem in vivo. Combining AP1S1 inhibition with anti-programmed cell death ligand 1 (anti-PD-L1) therapy exerted profound synergistic effects, driven by massive infiltration and functional activation of cytotoxic Granzyme B (GZMB)+CD8+ T cells.

CONCLUSIONS: Our study establishes the PCDsig we developed is a potential prognostic and predictive biomarker for breast cancer. We provide the first evidence of AP1S1 as a core immunomodulatory oncogene that mediates immune exclusion. Targeting AP1S1 represents a highly promising strategy to sensitize cold breast tumors to ICB, offering a new perspective for precision immunotherapy.

PMID:42712842 | PMC:PMC13551362 | DOI:10.21147/j.issn.1000-9604.2026.04.08

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An operational perturbation proteomics-based virtual cell model

Nature, Published online: 09 September 2026; doi:10.1038/s41586-026-11001-9

Temporal protein-abundance measurements from systematically perturbed breast cancer cell lines were generated to develop ProteinTalks, a virtual cell model that functions as an operational tool for diverse drug discovery tasks.
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