The c.7795_7797del variant in BRCA2 is predicted to cause a change in the length of the protein due to an in-frame deletion of 1 amino acid (p.(Glu2599del)). The Total GrpMax filtering allele frequency (the lower threshold of the 95% CI) in gnomAD v4.1 is 0.00000028 in the Non-Finnish European genetic ancestry group (based on 2/1179946 alleles) which is below the ENIGMA BRCA1/2 VCEP threshold (>0.00002) for BS1_Supporting and does not meet any population code (BA1, BS1, BS1_Supporting, PM2_Supporting are not met). This BRCA2 in-frame deletion variant is within a key functional domain and the computational predictor BayesDel (noAF) gives a score of 0.64, above the recommended threshold of 0.30 for prediction of impact on BRCA2 function via protein change. A SpliceAI score of 0.03 predicts no impact on splicing (score threshold ≤0.1) (PP3 met). Multifactorial likelihood ratio analysis using clinically calibrated data produced a combined LR for this variant of 2883172307.4 (based on Cosegregation LR=10545472; Pathology LR=0.93; Co-occurrence LR=1.03; Family History LR=285.42), above the thresholds for very strong evidence towards pathogenicity (LR >350) (PP4_Very strong met; PMID: 34597585, 31853058, 31131967). This is an in-frame variant inside a key functional domain. Impact via the protein change has not been assessed yet. mRNA experimental analysis indicates no impact on splicing (PMIDs: 22505045, 27886673) but is not applied as strong evidence against pathogenicity since missense impact has not been excluded (BP7_Strong (RNA) not met). 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 (PP3, PP4_Very strong).