EGFR and non-small cell lung carcinoma: While our findings thus underscore the role of GLUT1-mediated glucose metabolism in gefitinib resistance, it may be worth noting here that, consistent with a previous observation that GLUT1 loss alone (i.e., without EGFR inhibition) was sufficient to inhibit the proliferation of NSCLC cells [12], GLUT1 inhibition per se, either pharmacological or genetic, had growth inhibitory effects, albeit modest, on NSCLC cells also in our study.