As noted above, there is a known relationship between ARF6 and Rac1 and like podocyte-specific ARF6 null mice, Rac1 null mice also had no observable developmental or kidney abnormalities, whereas in vivo podocyte-specific deletion of CDC42, another Rho family small GTPase, resulted in proteinuria, effacement, and glomerulosclerosis [46]. This evidence concerns the gene RAC1 and glomerulosclerosis.