Although hyperactivating autophagy by a constitutively active BECN1 mutant (BECN1F121A) suppresses ER stress and improves systemic insulin sensitivity in response to high-fat diet feeding, it reduces insulin storage in pancreatic β cells and causes systemic glucose intolerance by excessive degradation of insulin granules, which can be reversed by treatment of autophagy inhibitors (Yamamoto et al., 2018). The gene discussed is BECN1; the disease is Glucose intolerance.