Indeed, we found in a recent study that AD-like tau accumulation could disrupt autophagosome-lysosome fusion by deregulating the Acidic nuclear phosphoprotein 32 family member A-Inhibitor of histone acetyl transferase-Increased sodium tolerance 1-Endosomal sorting complex required for transport III (ANP32A-INHAT-IST1-ESCRT-III) pathway, and this study preliminarily revealed a vicious cycle of tau accumulation and autophagy deficit in chronic AD neurodegeneration [19]. The gene discussed is ANP32A; the disease is Alzheimer disease.