ATG16L1 and Alzheimer disease: Furthermore, the same group also reported that the deletion of WD40 domain of ATG16L1, essential for LANDO or VAIL, is sufficient for driving spontaneous AD pathology including deposition of endogenous Aβ and hyperphosphorylated tau, microgliosis and neurodegeneration in aged (2 years old) mice in the absence of AD protein overexpression (Heckmann et al., 2020) These findings suggest that CASM, especially the VAIL pathway, is involved in age-associated neurodegenerative processes, which should be further analyzed.