Recent evidence indicates that BACE1 protein stability can be modulated by the lysosomal degradation pathway; in particular, caspase-3-dependent cleavage of Golgi-localized γ-ear-containing ARF-binding protein 3 (GGA3) is proposed to reduce BACE1 trafficking to the lysosome and thereby cause BACE1 elevation in AD [34]–[37]. Here, CASP3 is linked to Alzheimer disease.