What is strongly supported: ISR kinases phosphorylate eIF2alpha, limiting eIF2B-mediated ternary-complex recycling; ATF4/GCN4-like transcripts are selectively translated under low TC conditions.
What is context-dependent: Different kinases sense distinct stresses; chronic ISR can be adaptive or pathological, and recovery via GADD34/PPP1R15A matters.
What is weak, controversial, or assay-biased: Not all stress translation is ISR-dependent, and “cap-dependent blocked -> IRES active” can be too broad.
What may be duplicate biology under another name: Overlaps with DECOY, BYPASS, MATURE/UPR, SWITCH phosphorylation.
Missing or excessive graph structure
Missing edges: Add BRAKE -> VAULT for stress granule formation in many eIF2alpha-P contexts.
Excess edges: BRAKE -> BYPASS should be dashed/caveated; many proposed cellular IRES events are assay-sensitive.
Candidate splits: No split.
Candidate merges: No merge.
Candidate renames: ISR would be clearer.
Recommendation
Concrete graph change, if any: Keep; add stress-granule connection and caveat IRES activation.
Concrete technical-notes/blog wording change, if any: Mirror the graph recommendation in the glossary and relation catalogue, and explicitly mark the confidence/caveat where the claim is context-dependent or assay-sensitive.