NM_006206.5:c.1988C>T (p.Ala663Val) is a missense variant in exon 14 of PDGFRA, a receptor tyrosine kinase gene. This variant is absent from gnomAD v2.1 and v4.1 (0/1,607,834 alleles), meeting PM2 at supporting strength.¹ In silico analysis yields conflicting predictions: REVEL score of 0.755 suggests a damaging effect, but BayesDel (0.21064) and SpliceAI (max delta 0.00) predict a benign/no-impact outcome. Multiple lines of computational evidence do not converge on pathogenicity; PP3 is not met.² BayesDel and SpliceAI independently predict no deleterious effect, meeting BP4 at supporting benign strength.³ This variant is absent from ClinVar; no pathogenic or benign classification exists from any expert panel or clinical laboratory. PS1, PS5, PM5, PP5, and BP6 cannot be applied.⁴ No functional studies, de novo reports, case-control data, segregation data, or publications mentioning this specific variant were identified. PS2, PS3, PS4, PM6, PP1, PP4, BS2, BS3, BS4, BP2, and BP5 are not met.⁵ The variant is not located in a statistically significant mutational hotspot and no domain-level enrichment data support PM1. The gene-level PVS1 review does not provide robust evidence that PDGFRA disease is primarily caused by truncating variants; BP1 is not met. PVS1 is not applicable to this missense variant.⁶ PM2 (supporting pathogenic) and BP4 (supporting benign) are both met; the evidence is balanced and does not reach a classification threshold in either direction.⁷ Using the generic ACMG/AMP 2015 combination rules (Richards et al., PMID:25741868), one supporting pathogenic criterion (PM2) and one supporting benign criterion (BP4) result in a Variant of Uncertain Significance (VUS).⁸