Although mice do not have an APOL1 ortholog, the TgFVB mice recapitulates all of the clinical and molecular features of HIVAN [4–6], providing a model enabling for studying molecular mechanisms of glomerulosclerosis independent or downstream of APOL1. Murine susceptibility loci may also explain pathways leading to nephropathy in patients who do not harbor APOL1 risk alleles. The gene discussed is APOL1; the disease is HIV-associated nephropathy.