PN placement:ER proteostasis|Protein transport|Transmembrane protein import|EMC complex component ; PN-node mapping: type → GO:0072546 (EMC complex); group → GO:0044743 (protein transmembrane import into intracellular organelle); class → GO:0015031 (protein transport); branch=no_mapping.
Consistency: Deep research, review YAML, and PN annotation are consistent: EMC9 is the cytosolic, peripheral EMC8 paralog (mutually exclusive variant subunit), degenerate MPN domain, non-catalytic, docks via EMC2. The review carries the EMC9-specific developmental "foldopathy" evidence (PMID:37318954 — damaging EMC9 variants, neural-crest/WNT-Fzd7/β-catenin phenotype) not in the dossier; this is supporting, not contradictory.
PN story / NEW pressure: PN asserts only EMC membership + import/insertion, already captured (GO:0072546 part_of; the insertion/insertase terms KEEP_AS_NON_CORE since EMC8/EMC9 are interchangeable). No NEW GO term needed. The WNT-dependent developmental role is disease context, not a new molecular/process annotation; review correctly does not elevate it.
Mapping strategy:EMC9 does not change the shared node mapping (still an EMC complex member → GO:0072546). Same group-level issue as EMC7/EMC8: GO:0044743 (import into organelle interior) mismatches the EMC's membrane-protein insertion role; insertion terms are not subclasses of GO:0044743.
Evidence alignment: High overlap on the EMC insertase/structure core (22119785, 29242231, 32439656, 30415835, 32459176); review adds EMC9-specific PMID:37318954, 32332093 absent from the PN row but consistent with the membrane-protein-biogenesis framing.
Verdict: Consistent; well-reviewed. Note EMC9's contribution is via membership only (paralog-redundant), and the shared group→GO:0044743 mapping diverges from EMC insertion semantics.