Transgenic overexpression of the antiapoptotic Bcl-2 protein or targeted deletion of the proapoptotic gene Bax (Bcl-2-associated X protein) did not prevent neuronal loss and neurological disease in prion-infected mice [50, 51], neither did genetic ablation of caspase-12, a proposed mediator of ER stress-induced cell death [52]. Here, BAX is linked to nervous system disorder.