Failure explorer
Representative failures, not a highlight reel
D1 · Extract the gene/protein relationship(s) describing how BARD1 relates to BRCA1, with supporting evidence, from the corpus.
Agent1's own planner call returned syntactically invalid JSON (a real model error, not a parser bug: an extra closing bracket with no closing brace). The task failed outright, while Baseline1 answered it correctly on the same evidence.
What it said
parse_failure (planner): No JSON object found in planner response: '{"queries": ["BARD1 BRCA1 relationship", "BARD1 BRCA1 interaction", "BARD1 BRCA1 function"]]'
Gold evidence vs. what was retrieved
B4 · In which hematologic malignancies does the corpus describe TP53 status as prognostically significant, and for which is a specific patient population or predictive role noted?
BM25 missed both of B4's gold documents. The model correctly declined to answer given irrelevant evidence (a good outcome), but the task's expected_status is "supported" — real evidence exists in the corpus — so this is scored as an incorrect abstention. The root cause is retrieval, not reasoning.
What it said
The provided evidence does not describe TP53 status as prognostically significant in any hematologic malignancies. Additionally, there is no mention of a specific patient population or predictive role for TP53.
Gold evidence vs. what was retrieved
G1 · Does the corpus provide evidence that DDIAS directly binds or interacts with BRCA1?
The offline mock provider — which is architecturally incapable of fabricating a citation — still failed to abstain on this "insufficient evidence" trap task. BM25 retrieved a real, topically related document, and the extractive answer presented its content as if it addressed the specific relationship asked about. This never happened with the real live model (which correctly abstained on both G1 and G2, see the live trace linked from this task).
What it said
DNA double-strand breaks and unresolved DNA replication intermediates are particularly dangerous during mitosis. Paradoxically, cells inactivate canonical DNA repair mechanisms during chromosome segregation in favor of alternative pathways that depend on TOPBP1 and CIP2A, but how these pathways function is still poorly defined. Here, we describe the identification of DDIAS as a mitosis-specific DN