The c.7795G>A variant in BRCA2 is a missense variant predicted to cause substitution of Glutamic Acid by Lysine at amino acid 2599 (p.(Glu2599Lys)). This variant is absent from gnomAD v4.1 (read depth ≥25x in >90% samples, PM2_Supporting met). Reported by three calibrated studies to exhibit protein function similar to pathogenic control variants (PMIDs:38417439, 39779857, 39779848) (PS3 met). This BRCA2 missense variant is within a key functional domain. The computational predictor BayesDel (noAF) gives a score of 0.25, indicating that impact on BRCA2 function via protein change is unclear (score range 0.18-0.30) and the SpliceAI score of 0.17 indicates an unclear predicted impact on splicing (score range 0.10-0.20) (no bioinformatic code is applied). This variant has been detected in an individual with phenotype suggestive of BRCA2-Fanconi Anemia (FA). Clinical features of FA (no details reported) and Mitomicin-C (MMC)-induced chromosomal damage are seen in this individual. They were compound heterozygous for the variant and a pathogenic or likely pathogenic variant (BRCA2:c.7890_7891dup, p.Leu2631HisfsTer18) inferred to be in trans, phase was unknown. Total points equated to 1 (PM3_Supporting met; PMID: 23285130). In summary, this variant meets the criteria to be classified as a Likely pathogenic variant for BRCA2-related cancer predisposition based on the ACMG/AMP criteria applied as specified by the ENIGMA BRCA1/2 VCEP (PM2_Supporting, PS3, PM3_Supporting).