Clinical trials using drugs targeting EGFR kinases have not had very successful outcomes due to various factors including adaptation to dose‐limiting drug toxicity.9 NHE9 overexpression in glioblastoma cells was shown to greatly decrease the efficacy of erlotinib, a known FDA‐approved tyrosine kinase inhibitor of EGFR.4 The goal of this study was to integrate the knowledge gained from our previous investigations into NHE9 function, to significantly improve the efficacy in the treatment of the subset of GBM associated with NHE9 overexpression (henceforth referred to as GBM9+). This evidence concerns the gene SLC9A9 and glioblastoma.