AKT1 and hereditary disease: Palmieri M et al. [81, 82] reported that TFEB activity is modulated by AKT phosphorylation at Ser467, and both AKT knockdown and the pharmacological inhibition of AKT promoted the nuclear translocation and stability of TFEB, as well as increased its ability to activate downstream target genes, thus promoting cellular clearance in a variety of models of genetic diseases, including patient-derived primary fibroblasts defective for PPT1, and TPP1M, and MFSD8, presenting with an impairment of lysosomal pathways (Fig. 4).