The selective deletion of neuronal Nhe1 (in CamKIIa-Cre+/−; Nhe1flox/flox mice) or astrocytic Nhe1 (in Gfap-CreER+/−; Nhe1flox/flox mice) both showed a significantly reduced ischemic infarct and accelerated neurological functional improvements in a mouse tMCAO model [13,23], while the targeted deletion of microglial Nhe1 in Cx3cr1-CreER+/−; Nhe1flox/flox mice did not reduce infarct but improved motor-sensory and cognitive behaviors with mitigated acute inflammation and enhanced long-term myelination up to 1 month after ischemic stroke [13,26]. Here, SLC9A1 is linked to ischemic stroke.