SLC2A1 and non-small cell lung carcinoma: A hypothetical scenario could therefore be envisaged whereby EGFR inhibitors elicit in NSCLC cells a growth-inhibitory signal(s) subject to the GLUT1-dependent resistance mechanism, which is inactivated by EGFR inhibitors in NSCLC cells with activating mutations but not in those without, which then leads to the differential sensitivity of NSCLCs with and without activating EGFR mutations to EGFR inhibitors.