NM_000465.4:c.1835A>T (p.Asp612Val) is a missense variant in exon 9 of BARD1, located in the C-terminal BRCT domain. It is rare in population databases, with an allele frequency of 0.012% in gnomAD v4.1 (199/1,613,842 alleles, 0 homozygotes).¹ Functional data from a published homology-directed repair assay (PMID:30925164) demonstrated that p.Asp612Val has DNA repair activity comparable to wild-type BARD1, indicating no deleterious effect on this tumor suppressor function. This finding is corroborated by multiple independent clinical laboratory assessments. Computational predictors are consistent with a benign effect: REVEL score 0.27 and BayesDel score -0.224875 both predict a benign impact. While SpliceAI delta score is 0.65, this is not corroborated by the protein-level in silico tools.² BARD1 disease mechanism is loss-of-function through truncating variants; missense variants without demonstrated functional impact are less likely to be pathogenic. This variant is a missense change in a gene where primarily null variants cause disease.³ In ClinVar, this variant has conflicting classifications: 9 clinical laboratories report it as Uncertain Significance and 5 report it as Likely Benign. No expert panel has reviewed this variant. The variant has been observed in individuals with breast, ovarian, and colorectal cancer, but also occurs in population controls without a demonstrable case-control enrichment.⁴ Applying ACMG/AMP 2015 criteria: PM1 (supporting, BRCT domain), PM2 (supporting, rare in population) are met for pathogenic evidence. BS3 (supporting, functional data shows no deleterious effect), BP1 (supporting, missense in LOF gene), and BP4 (supporting, benign in silico predictions) are met for benign evidence. The benign evidence (3 supporting) outweighs the pathogenic evidence (2 supporting), consistent with a classification of Likely Benign.⁵