These data not only corroborated our findings that Nhe1 cKO specifically expanded the MG3 subgroup associated with increased SPP1 pathways involved in myelin-supporting functions of microglia, but also unveiled possible novel mechanisms of the Psap-Gpr37 ligand-receptor pairs in promoting white matter repair in post-stroke Nhe1 cKO brains. This evidence concerns the gene SLC9A1 and stroke disorder.