Importantly, disturbance of the autophagy flux in podocytes, by podocyte‐specific deletion of Atg5 (Hartleben et al, 2010), Pik3c3/Vps34 (Bechtel et al, 2013), or Ctsd (cathepsin D) (Yamamoto‐Nonaka et al, 2016), underpins events of glomerulosclerosis and proteinuria, culminating in severe glomerulopathy and kidney dysfunction. This evidence concerns the gene ATG5 and lipoprotein glomerulopathy.