The strong epidemiologic association between high-risk APOL1 genotype and COVAN has led to the hypothesis that COVID-19–induced expression of APOL1 G1 or G2 in podocytes and glomerular endothelial cells (GECs) — the kidney cells affected in collapsing glomerulopathy — drives pathogenesis of COVAN. The gene discussed is APOL1; the disease is COVID-19.