The prevailing hypothesis that APOL1 risk variant-driven cation influx likely drives podocyte cytotoxicity is strongly supported by the impressive decrease in proteinuria of African Americans with focal segmental glomerulosclerosis (FSGS) in a phase II trial of Vertex’s small molecule inhibitor of APOL1 channel function (VX-147, Inaxaplin)5. Here, APOL1 is linked to focal segmental glomerulosclerosis.