The strength of our study is that it provides one instance of an inconsistency with the prevailing theory for APOL1: if the G1 and G2 alleles predispose to glomerulosclerosis in a recessive model, suggesting a loss of function mutation, then a gentleman with a canonical loss of function mutation (a null allele) should have at least as high a predilection for kidney disease. This evidence concerns the gene APOL1 and glomerulosclerosis.