NM_005732.3:c.2301dup (p.Ile768HisfsTer14) is a frameshift duplication in exon 14 of RAD50, predicted to undergo nonsense-mediated decay. RAD50 loss of function is an established disease mechanism for RAD50 deficiency syndrome.¹ The variant is absent from gnomAD v2.1, v4.1, and gnomAD-Canada, consistent with a rare pathogenic variant.² No variant-specific functional data, clinical case reports, de novo observations, or segregation data were identified in the reviewed literature. Four RAD50 gene-level publications were reviewed but none reported this specific variant. Under generic ACMG/AMP 2015 combination rules (PMID:25741868), one strong criterion (PVS1) plus one supporting criterion (PM2) yields a classification of Likely Pathogenic.³