PVS1 is met at Very Strong strength: this is a frameshift deletion in BRCA2 exon 11 predicted to truncate the protein at residue 2186 of 3418, well upstream of the final exon, in a gene where the ENIGMA CSPEC establishes germline loss of function as the disease mechanism and applies PVS1 at default Very Strong strength for such null variants, with no bundle evidence of NMD escape, exon-skip rescue, or exclusion for this exon. PM4 and BP3 are both not_applicable: the governing ENIGMA BRCA1/BRCA2 VCEP Specification v1.2 explicitly excludes both criteria for BRCA2 gene-wide, and independently this frameshift variant does not fit either criterion's underlying variant-type requirements (in-frame length change / in-frame repeat-region indel). NM_000059.4:c.6546_6574del is a frameshift/PTC-producing 29-bp deletion (p.(K2182Nfs*5)) in BRCA2 exon 11, not a missense or in-frame variant, which removes it from the scope of the classic residue/domain criteria as written in the governing ENIGMA BRCA1/BRCA2 CSPEC v1.2. PM1 and PP2 are globally marked 'Not Applicable' for BRCA2 in the ENIGMA CSPEC v1.2, independent of variant type. PS1 and BP1 are scoped by the CSPEC to missense/silent/in-frame or splicing-impact variants and do not apply to this out-of-frame frameshift deletion. PM5 is repurposed by the CSPEC into a PM5_PTC exon-based rule; exon 11 is confirmed PM5_PTC-eligible (not on the BRCA2 PM5_N/A exon list of E6/E12/E27), but the case bundle's Table 4 excerpt does not resolve the specific per-exon strength code or a comparator previously-proven pathogenic PTC variant, so PM5 is left not_assessed pending review of the full Specifications Table 4 spreadsheet. Variant NM_000059.4:c.6546_6574del / NP_000050.3:p.(Lys2182AsnfsTer5) is a 29 bp frameshift deletion in BRCA2 exon 11, a null/PTC-generating variant type. The ENIGMA ClinGen BRCA1/2 v1.2 specification's PS3/BS3 functional-assay track (Specifications Table 9) is explicitly scoped to missense and synonymous variants and mRNA-transcript (splicing) assays; it does not cover frameshift/deletion null variants, whose loss-of-function status is instead assessed via PVS1 (handled outside this group). No calibrated protein-function or mRNA/minigene assay result specific to this exact deletion was found in Specifications_Table9_V1.2_2024-11-18, HUMU-40-1557-s001 (Parsons 2019), or any fetched full-text publication in this case bundle. Both PS3 and BS3 are therefore returned as not_assessed rather than not_applicable, since the ENIGMA framework does in principle allow functional evidence for null variants via the mRNA-assay/PVS1(RNA) pathway — that pathway simply has no variant-specific data available in this case. NM_000059.4:c.6546_6574del is a 29-bp coding deletion (not a multiple of 3) producing a frameshift, NP_000050.3:p.(Lys2182AsnfsTer5) / p.(K2182Nfs*5), per case_summary.json normalization. The governing ClinGen ENIGMA BRCA1/BRCA2 v1.2 specification (cspec) scopes its PP3/BP4/BP7 bioinformatic-code rules to specific variant categories only: missense or in-frame insertion/deletion/delins inside a functional domain (BayesDel no-AF thresholds), silent variants (SpliceAI thresholds), and intronic variants outside the canonical +/-1,2 splice positions (SpliceAI thresholds). A frameshift-causing out-of-frame exonic deletion is not among these categories and instead falls under the PVS1 null-variant pathway (assessed by a different criteria group), so PP3, BP4, and BP7 are all not_applicable for this variant. SpliceAI was independently checked as a sanity check: max delta score = 0.009 (all four delta scores <=0.009), indicating no significant predicted splicing perturbation even if a splicing-based path had been eligible. REVEL and BayesDel scores were not computed/available for this variant in evidence.json (both null), and per pipeline policy BayesDel lacks a verified published calibration threshold regardless, so neither could support PP3/BP4 even under a hypothetical missense/in-frame-indel framing. No literature (paper_extracts.json) discusses this specific variant's splicing or in-silico predictions; the five full-text papers reviewed are gene-level functional/mechanism papers that do not mention c.6546_6574del.