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Can AI Agents Detect and Repair Artifact Drift in Network Experiments?

arXiv:2609.09849v1 Announce Type: cross Abstract: In recent years, AI agents have evolved into capable assistants that carry out multi-step tasks in digital environments. The network systems community is beginning to explore these capabilities in operational and experimental settings. However, an agent operating in network systems should not be judged solely by whether it completes the immediate task. The experiment record it modifies must also remain trustworthy. We call this property artifact integrity: the record's claims must remain supported by the available evidence, confined to the scope established by that evidence, and traceable through the artifacts that encode their support. To make this property measurable, we introduce NetArtifactBench, which tests whether AI agents can repair inconsistent records derived from public network-system artifacts while preserving claims that remain supported. The benchmark contains 52 instances with injected inconsistencies ranging from direct contradictions to unstated relations spread across several artifacts. We evaluate 23 agent configurations across three general-purpose AI agent runtimes using deterministic scoring. The average contract pass rate is 65.3 % across 5,980 outputs, but no agent runtime exceeds 30 % when repair requires recovering implicit relations and propagating changes across artifacts. These results reveal a sharp boundary between local correction and complete record-level repair. Therefore, we argue that artifact integrity should become a first-class design and evaluation requirement for AI agents operating on network systems.

MCAT-mediated mitochondrial fatty acid metabolism regulates Lauren subtype divergence and suppresses gastric cancer progression through ROS/P53-dependent mitophagy and ferroptosis

9 September 2026 at 18:00

Cell Death Differ. 2026 Sep 8. doi: 10.1038/s41418-026-01867-7. Online ahead of print.

ABSTRACT

Gastric cancer (GC) displays marked heterogeneity under the Lauren classification, yet the metabolic determinants of subtype divergence remain unclear. Here, we identify Malonyl-CoA:ACP transacylase (MCAT), a Lauren subtype-associated gene encoding a key mitochondrial fatty acid synthesis (mtFAS) enzyme, as a subtype-specific tumor suppressor in GC. Integrative multi-omics profiling revealed that MCAT expression is enriched in intestinal-type GC and correlates with favorable prognosis. Mechanistically, MCAT overexpression drives metabolic reprogramming through mitochondrial free fatty acid overload, suppressing Ξ²-oxidation while elevating mitochondrial reactive oxygen species (ROS), which triggers P53 phosphorylation at Ser15. This event concurrently activates PINK1/Parkin-mediated mitophagy and suppresses the SLC7A11/GPX4 axis to induce ferroptosis. Genetic rescue experiments confirmed that P53-Ser15 phosphorylation is essential for both mitophagy and ferroptosis induction. Endogenous MCAT levels are sufficient to determine basal ROS/P53/mitophagy/ferroptosis axis activity, and knockdown in high-expressing cells reverses these phenotypes, supporting a physiological, threshold-dependent role. In vivo, MCAT overexpression suppresses tumor growth and enhances mitophagy and ferroptosis markers. Collectively, these findings establish MCAT as a metabolic switch that links mtFAS to ROS/P53-dependent cell death, providing a potential biomarker and therapeutic target for GC.

PMID:42711380 | DOI:10.1038/s41418-026-01867-7

MCAT-mediated mitochondrial fatty acid metabolism regulates Lauren subtype divergence and suppresses gastric cancer progression through ROS/P53-dependent mitophagy and ferroptosis

Cell Death Differ. 2026 Sep 8. doi: 10.1038/s41418-026-01867-7. Online ahead of print.

ABSTRACT

Gastric cancer (GC) displays marked heterogeneity under the Lauren classification, yet the metabolic determinants of subtype divergence remain unclear. Here, we identify Malonyl-CoA:ACP transacylase (MCAT), a Lauren subtype-associated gene encoding a key mitochondrial fatty acid synthesis (mtFAS) enzyme, as a subtype-specific tumor suppressor in GC. Integrative multi-omics profiling revealed that MCAT expression is enriched in intestinal-type GC and correlates with favorable prognosis. Mechanistically, MCAT overexpression drives metabolic reprogramming through mitochondrial free fatty acid overload, suppressing Ξ²-oxidation while elevating mitochondrial reactive oxygen species (ROS), which triggers P53 phosphorylation at Ser15. This event concurrently activates PINK1/Parkin-mediated mitophagy and suppresses the SLC7A11/GPX4 axis to induce ferroptosis. Genetic rescue experiments confirmed that P53-Ser15 phosphorylation is essential for both mitophagy and ferroptosis induction. Endogenous MCAT levels are sufficient to determine basal ROS/P53/mitophagy/ferroptosis axis activity, and knockdown in high-expressing cells reverses these phenotypes, supporting a physiological, threshold-dependent role. In vivo, MCAT overexpression suppresses tumor growth and enhances mitophagy and ferroptosis markers. Collectively, these findings establish MCAT as a metabolic switch that links mtFAS to ROS/P53-dependent cell death, providing a potential biomarker and therapeutic target for GC.

PMID:42711380 | DOI:10.1038/s41418-026-01867-7

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