The variant affects the canonical +2 donor position of CHEK2 and is expected to disrupt normal splicing, which supports PVS1 in a loss-of-function disease mechanism context.¹ The reviewed CHEK2 framework mode is VCEP and the case workspace points to the CHEK2 ClinGen specification as the primary interpretive authority, although the local criterion table was not populated.² Population data support rarity: the variant is absent from gnomAD v2.1 and observed only once in gnomAD v4.1 with no homozygotes, supporting PM2 at supporting strength.³ No convincing variant-specific case-control, segregation, de novo, or functional RNA evidence for this exact allele was identified in the reviewed workspace, so no additional criteria were added. Using ACMG/AMP combining rules, PVS1 plus PM2_Supporting supports a Likely Pathogenic classification.⁴