Given the high WDR4 expression and the low PTPN23 expression in lung cancers as well as the suppressive effect of WDR4/PTPN23 axis on EGFR and c-MET lysosomal degradation, we reasoned that disruption of the interaction between WDR4 and PTPN23 would stabilize PTPN23 to promote EGFR and c-MET trafficking to lysosome for degradation, thereby suppressing NSCLC malignancies and EGFR TKI resistance. The gene discussed is EGFR; the disease is lung cancer.