Transgenic mice lacking the DAPK1 gene or with mutated GluN2B C-terminal region abolishing GluN2B-DAPK1 binding is resistant to ischemic insult during in vitro and in vivo models of stroke (see Tu et al., 2010; Tang et al., 2018 but McQueen et al., 2017), while interfering the formation of the GluN2B-DAKP1 complex using cell-penetrant peptides Tat-GluN2Bct and Tat-GluN2Bct-CTM is neuroprotective against mice models of ischemic stroke (Tu et al., 2010; Fan et al., 2014). This evidence concerns the gene TAT and stroke disorder.