In recent studies, we reported that selective deletion of microglial Nhe1 in the Cx3cr1-CreER±;Nhe1flox/flox (cKO) mice reduced proinflammatory responses at 3 days post-stroke [12] and improved oligodendrogenesis along with remyelination tested at 3, 14, and 28 days post-stroke in the Nhe1 cKO mice [13]. This evidence concerns the gene SLC9A1 and stroke disorder.