The existence of the remaining 20% to 30% of patients with COVAN (or HIVAN) who do not carry high-risk APOL1 genotypes suggests the possibility of an APOL1-independent pathomechanism or the possibility that, in some cases, COVID-19–induced supraphysiologic expression of G0 APOL1 may also cause podocytopathy. The gene discussed is APOL1; the disease is HIV-associated nephropathy.