Moreover, restoring lysosomal proteolytic activity by deletion of cystatin b, an endogenous inhibitor of certain lysosomal cysteine proteases of the cathepsin family, rescues autophagy flux blockade in neurons, diminishes Aβ load, and prevents learning and memory deficits in an amyloid precursor protein (APP)-overexpressing TgCRND8 mouse model of AD [54]. The gene discussed is APP; the disease is Alzheimer disease.