While our study identifies a novel APOL1 variant associated with FSGS and provides functional evidence for its pathogenicity, several limitations warrant acknowledgment: The absence of extended familial segregation precludes definitive confirmation of its de novo origin; lack of systematic screening for podocytopathy genes (NPHS1, NPHS2, INF2, etc.)prevents exclusion of alternative genetic contributors. This evidence concerns the gene NPHS1 and focal segmental glomerulosclerosis.