We show that APOL1 BAC transgenic mice homozygous for the risk variants G1 and G2, but not G0, develop overt kidney disease in response to IFN-γ, which is characterized by high albuminuria, increased serum creatinine and BUN, glomerulosclerosis and podocyte loss, and eventual death. The gene discussed is IFNG; the disease is glomerulosclerosis.