c.507G>A is a silent (synonymous) substitution in BRCA1 exon 7 producing p.Gln169= (NP_009225.1:p.(Q169=)). BP1_Strong is met: the variant is a silent substitution at residue 169, which is outside all three BRCA1 clinically important functional domains (RING aa2-101, coiled-coil aa1391-1424, BRCT repeats aa1650-1857), and SpliceAI predicts no splicing impact (max delta 0.01).¹ The variant is present at very low frequency in gnomAD population databases (v2.1: 3/282870 alleles; v4.1: 28/1613772 alleles) but does not meet BS1 or BA1 thresholds.² PVS1, PS1, PS5, PM5, and BP4 are not applicable due to the silent nature of the variant. PP3 is not met (SpliceAI 0.01 < 0.2). PM2 is not met (variant is present in gnomAD).³ PS3, BS3, and BP7 remain not assessed pending verification of a reported minigene splicing assay (Fraile-Bethencourt et al. 2017) that found no splicing aberration. Confirmation of this finding would support BS3 and BP7. PP4 and BP5 are not assessed because the variant is not represented in the Li et al. 2020 (PMID:31853058) clinical-history likelihood ratio table or the Parsons et al. 2019 multifactorial dataset.⁴ ClinVar reports an ENIGMA expert panel classification of Likely benign (ClinVar ID 185706, review status: reviewed by expert panel). The ENIGMA classification likely incorporates the minigene splicing evidence and/or additional clinical data not captured in the available VCEP spreadsheets.⁵ Under strict ENIGMA Table 3 combining rules, BP1_Strong alone is insufficient to reach Likely Benign without at least one additional supporting benign criterion of a different evidence type. The available data therefore place this variant between Likely Benign (per ENIGMA expert panel classification) and VUS (per strict criteria-based adjudication without verified BS3/BP7).⁶