In our recent studies in Alzheimer’s Disease, using wild type and genetically modified HCT116 colon cancer cells as a model system expressing either ATG16L1 T300 or ATG16L1 A300, we determined whether drugs that directly inhibit the chaperone ATPase activity or cause chaperone degradation and endoplasmic reticulum stress signaling leading to macroautophagy could reduce the levels of proteins which play a pathogenic role in neurodegenerative diseases [10]. The gene discussed is ATG16L1; the disease is Alzheimer disease.