We further tested our hypothesis by assessing the impact of selective deletion of Nhe1 in Cx3cr1+ cells on changes of glioma immunity in a nonimmunogenic SB28 GBM model which recapitulates key characteristics of human GBM including low mutational load, a factor believed to be responsible for immune checkpoint therapy resistance 30. The gene discussed is SLC9A1; the disease is glioblastoma.