While other post-translational mechanisms may account for this observed decrease in GGA3, it is tempting to speculate that apoptotic events may play a role in the increase in BACE1 in AD brain, indeed, elevated BACE1 activity may lead to increased Aβ levels and, given that Aβ can induce apoptosis, this could potentially trigger a vicious cycle that self-potentiates Aβ generation and cell death. The gene discussed is BACE1; the disease is Alzheimer disease.