Namely, downregulation of GluN1 in podocytes in culture and in glomeruli led to a marked increase of Cdc42-GTP levels, with no changes in levels of RhoA and Rac1, after in vitro high-glucose exposure or in vivo induction of diabetes, supporting a direct inhibitory role of NMDARs on Cdc42 activation [101]. The gene discussed is CDC42; the disease is diabetes mellitus.