The observed ability of FD22a to promote TFEB nuclear entry by dephosphorylation of S211, the target serine of mTOR, followed by TFEB-mediated activation of autophagic lysosomal function, associated with the ability to prevent β-amyloid-induced cytotoxic and proinflammatory effects, may have a marked relevance in the prevention and/or treatment of AD pathology. Here, MTOR is linked to Alzheimer disease.