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DRIVE: Modeling Skills at the Reasoning and Interaction Levels for Web Agents under Continual Learning

arXiv:2605.23939v1 Announce Type: new Abstract: Web agents require both high-level reasoning (for task decomposition) and low-level interactions (for page elements manipulation) to conduct different tasks. However, these knowledge types differ fundamentally: reasoning knowledge (e.g., booking a flight requires first searching for routes) is abstract and transferable across websites, while interaction knowledge (e.g., clicking the Search button at a specific coordinate on Site A) depends heavily on page-specific contexts. Existing methods store experiences uniformly. This creates a dilemma: abstract representations lose executability on concrete pages, while concrete representations fail to generalize across domains. This entanglement limits capability accumulation: on new websites, agents either fail to recognize reusable task logic due to surface-level differences or attempt infeasible actions from outdated page structures. To disentangle them, we propose DRIVE, a dual-level skill modeling framework separating historical experience into natural language reasoning skills, which capture transferable task logic, and programmatic interaction skills, grounding abstract actions to executable operations. A scene-aware coordination mechanism adaptively retrieves and invokes these dual-level skills based on task semantics. DRIVE also uses skill-level reflection to identify hierarchy-specific failure modes, enabling targeted skill library expansion and refinement. Experiments across five WebArena domains show DRIVE attains an average task success rate of 52.8%, exceeding the skill-free baseline by 7.3 percentage points. Further ablations show reasoning and interaction skills provide distinct, complementary benefits, supporting separation of transferable task logic from executable page-level operations.

Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing

Oncogene, Published online: 18 April 2026; doi:10.1038/s41388-026-03781-1

Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing

Multi-Omics and Single-Cell Mendelian Randomization Reveal a Potential Role of VNN2 in Lung Adenocarcinoma in Resting Natural Killer Cells

13 March 2026 at 18:00

World J Oncol. 2026 Mar 5;17(2):247-255. doi: 10.14740/wjon2689. eCollection 2026 Apr.

ABSTRACT

BACKGROUND: We aimed to evaluate the potential association between genetically predicted vanin-2 (VNN2) expression and lung adenocarcinoma (LUAD) risk, and to explore the immune cell subtype that may underlie this relationship.

METHODS: We integrated whole-blood expression quantitative trait loci (eQTL) data from eQTLGen, plasma protein quantitative trait loci (pQTL) data from deCODE, and LUAD genome-wide association study (GWAS) data from European-ancestry cohorts, together with differential expression analysis using GEPIA2, to identify candidate genes for subsequent single-cell eQTL (sc-eQTL) Mendelian randomization (MR) analysis. For the sc-eQTL analysis, VNN2-associated eQTLs from 14 immune cell types profiled in the OneK1K single-cell eQTL resource were tested for associations with LUAD risk.

RESULTS: Bulk-level MR analysis showed that genetically predicted increases in VNN2 expression and protein levels were significantly associated with a reduced risk of LUAD (eQTL-MR: odds ratio (OR) = 0.964, 95% confidence interval (95% CI), 0.934-0.995; P = 0.024; pQTL-MR: OR = 0.946, 95% CI, 0.921-0.970; P = 2.87 Γ— 10-5). Transcriptomic analyses confirmed significant downregulation of VNN2 in LUAD tumors compared with normal lung tissues. sc-eQTL MR identified the strongest association in resting natural killer (rNK) cells (OR = 0.896, 95% CI, 0.829-0.967; P = 0.005).

CONCLUSIONS: Multi-omics and sc-eQTL MR analyses indicated that genetically predicted increases in VNN2 expression were associated with a reduced risk of LUAD, with the most pronounced effect observed in rNK cells. These findings suggest a potential cell type-specific role of VNN2 in LUAD susceptibility and warrant further studies to validate its biological relevance and clinical implications.

PMID:41822323 | PMC:PMC12978397 | DOI:10.14740/wjon2689

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