Genetic or pharmacological inactivation of GSK3β promotes the nuclear accumulation of TFEB to induce lysosomal biogenesis and autophagy, leading to a reduction in Aβ1-42 and phosphorylated tau levels and subsequent amelioration of cognitive deficits in AD murine models [3, 84, 85] (Fig. 3B). Here, GSK3B is linked to Alzheimer disease.