PN placement: three ALP rows — mTORC1-upstream/insulin/TSC-deactivator; FOXO transcriptional-program modulator; and Chaperone-mediated autophagy|...|CMA inhibitor|Modulator of LAMP2A multimerization ; PN-node mapping: TSC and FOXO subtrees no_mapping / context_only (too_broad, GO:0010506); CMA-inhibitor type mapped→GO:1904715 (negative regulation of CMA, propagate). Projection: GO:1904715 more_specific_than_existing_goa.
Consistency: Consistent across layers. Deep research (falcon) frames AKT1 as the PI3K-AKT Ser/Thr kinase; PN notes capture TSC2, GFAP/LAMP2, FOXO1/3, and LAMP2A-multimerization CMA inhibition. Review adopts only the CMA-inhibitor projection (action NEW GO:1904715, IMP, PMID:26118642) and keeps TSC/FOXO/autophagy roles as non-core kinase outputs. No contradiction.
PN story / NEW pressure: PN asserts directional CMA inhibition not specifically in GOA (GOA has only broad GO:0010507 negative regulation of autophagy). GO:1904715 verified real (child of GO:0010507 + GO:1904714); GOA confirms it is genuinely more-specific/new. Direct support from lysosomal mTORC2/PHLPP1/Akt CMA assays (PMID:26118642). Verdict: ADD — defensible refinement of the existing broad term.
Mapping strategy: No node change. The mapping correctly restricts propagation to the CMA-inhibitor type (directional GO:1904715) rather than projecting the class-level GO:0061684 chaperone-mediated autophagy (which would wrongly make AKT1 a direct CMA participant). The LAMP2A-multimerization subtype stays no_mapping/contextual — appropriate. PN-projected term is correctly scoped (narrower than class, not over-broad).
Evidence alignment: Good overlap. PN reference titles (Lysosomal mTORC2/PHLPP1/Akt = PMID:26118642; Akt/FoxO; TSC2-Akt) map onto review references PMID:26118642, 12172553, FOXO PMIDs. CMA-collapse and CMA-motif papers cited in PN are background, not load-bearing for the GO:1904715 call.
Verdict: Consistent; GO:1904715 ADD confirmed (realized as NEW in review). TSC/FOXO correctly kept as non-core.