Overexpressing of anti-apoptotic BCL2 in the postmitotic neurons of an AD mouse models reduced the activation of caspase 9 and caspase 3, thereby limiting the caspase-mediated cleavage of tau and the formation of neurofibrillary tangles.452 Furthermore, the neurons of these mice showed increased intracellular accumulation of amyloid precursor protein, thus restricting the formation of Aβ plaques. The gene discussed is BCL2; the disease is Alzheimer disease.