The activation of eNMDARs leads to cell death by inhibiting survival signaling as well as promoting pro-death mechanisms such as the expression of cleaved caspase-3 [153, 197], the suppression of the CREB, p38 MAPK, and ERK1/2 pathways [190, 198], the activation of the FOXO transcription factor associated with AD neuropathology [191], and calpain-mediated cleavage of striatal-enriched protein tyrosine phosphatase (STEP) [79, 195, 199–201] (Figs. 3 and 4). This evidence concerns the gene CREB1 and Alzheimer disease.