This variant is an intronic substitution at c.211+9 in MSH2, located beyond the +7 splice boundary, meeting BP7 (supporting benign).¹ SpliceAI predicts no splicing impact (max delta = 0.00), meeting BP4 (supporting benign) for intronic variants under the InSiGHT MSH2 VCEP (Walker et al. 2023).² This variant is present at extremely low frequency in gnomAD v4.1 (overall AF = 5.04 × 10⁻⁶, 8/1,588,690 alleles, 0 homozygotes), meeting PM2 at supporting strength under the InSiGHT MSH2 VCEP threshold of <0.00002.³ The grpmax filtering allele frequency in gnomAD v4.1 is 8.99 × 10⁻⁵ (0.009%), which is below the BS1 threshold (≥ 0.0001) and the BA1 threshold (≥ 0.001); therefore BS1 and BA1 are not met.⁴ PVS1 is not applicable — this is an intronic variant at +9, not a null variant or canonical splice site variant under the InSiGHT MSH2 VCEP PVS1 decision tree.⁵ No tumor MSI/IHC, co-segregation, de novo, functional assay, or case-control data are available for this variant. No publications specifically report NM_000251.3:c.211+9C>A. Under the InSiGHT MSH2 VCEP v2.0.0 combining rules, two supporting benign criteria (BP4, BP7) meet Rule 19 (≥ 2 Benign Supporting → Likely Benign). One pathogenic supporting criterion (PM2) is also present but does not trigger a VCEP-defined conflict with benign supporting evidence.⁶