Podocyte-specific deletion of a gene coding autophagy protein 5 (Atg5) led to a glomerulopathy in ageing mice that was accompanied by an accumulation of oxidized and ubiquitinated proteins, endoplasmic reticulum (ER) stress, and proteinuria, which ultimately resulted in podocyte loss and late-onset glomerulosclerosis 2. The gene discussed is ATG5; the disease is lipoprotein glomerulopathy.