In common with other terminally differentiated cell types, podocytes have a high level of autophagy under basal conditions32 and impairment of this process has been implicated in podocyte damage associated with aging,35, 42, 43 diabetic nephropathy,34 mitochondrial dysfunction and FSGS.33 Conversely, enhancement of autophagic activity has a protective effect in models of glomerular disease.36, 44 As global GSK3α knockout has been found to impair autophagy in multiple organ systems, we surmised that GSK3α knockout podocytes might also be autophagy deficient. This evidence concerns the gene GSK3A and glomerular disorder.