However, maybe because the wild‐type EGFR possess lower affinity for gefitinib than that of the Exon19 del/L858R mutant,38, 39 the IC50 of gefitinib in glioma cells both in our study and others40 was higher than those in other type of cancers such as NSCLC with EGFR mutation.38 Therefore, it is hard to directly examine the clinical response of gefitinib in GBM patients with high GOLPH3 now. The gene discussed is GOLPH3; the disease is glioma.