Moreover, transactivation of TFEB transcriptional targets may limit the accumulation of beta‐amyloid either by increasing autophagic degradation of the amyloid precursor protein (APP), or by increasing (Parr et al, 2012) the clearance of toxic amyloid (beta) aggregates in some (Xiao et al, 2015), but not all (Oakley et al, 2006; Polito et al, 2014), mouse models of Alzheimer's disease. This evidence concerns the gene APP and Alzheimer disease.