Previous studies have shown that NHE9 overexpression exerts post‐translational control by increasing persistence of EGFRs on glioblastoma cell membranes, by attenuating receptor turnover significantly.4 Consistent with increased membrane persistence of EGFRs, efficacy of erlotinib, an FDA‐approved receptor tyrosine kinase inhibitor of EGFR, is significantly reduced. The gene discussed is NTRK1; the disease is glioblastoma.