The variant NM_001354609.1:c.1068A>G (p.Gln356=) is a synonymous substitution in BRAF exon 8, outside the critical functional domains defined by the ClinGen RASopathy VCEP.¹ This variant is present in gnomAD v2.1 at an allele frequency of 0.02546% (72/282,848 alleles, 1 homozygote) with a grpmax filtering allele frequency of 0.1388%, and in gnomAD v4.1 at 0.01394% (225/1,614,110 alleles, 2 homozygotes) with a grpmax FAF of 0.1350%.² BA1 is met at stand-alone benign strength: the gnomAD grpmax FAF of 0.1388% (v2.1) and 0.1350% (v4.1) exceeds the CSPEC RASopathy VCEP threshold of ≥0.05%.³ BS1 is met at strong benign strength: the gnomAD grpmax FAF exceeds the CSPEC RASopathy VCEP threshold of ≥0.025%.⁴ BS2 is met at strong level: homozygous individuals are observed in gnomAD (1 in v2.1, 2 in v4.1), which is inconsistent with a highly penetrant autosomal dominant RASopathy disorder.⁵ BP4 is met at supporting benign strength: SpliceAI predicts no significant splice impact (max delta 0.01), satisfying the VCEP BP4 criterion for negligible predicted splicing outcome.⁶ BP7 is met at supporting benign strength: the variant is synonymous (p.Gln356=) with no predicted splice impact (SpliceAI delta 0.01), applied in conjunction with BP4.⁷ The ClinGen RASopathy Variant Curation Expert Panel has classified this variant as Benign (ClinVar Variation ID 44788), applying criteria BA1, BS1, BP4, and BP7, consistent with this independent assessment.⁸ Under the CSPEC RASopathy VCEP v2.3.0 classification framework Rule 17, BA1 alone (stand-alone benign) is sufficient for a Benign classification. Additionally, BS1 (strong) and BS2 (strong) satisfy Rule 16 (≥2 strong benign criteria). The variant is classified as Benign.⁹