Our demonstration that GLUT1 has pivotal roles in the growth and gefitinib resistance of NSCLC cells, combined with the observation that GLUT1 expression and glucose uptake were increased in resistant NSCLC cells after gefitinib treatment, may give rise to a hypothesis that the differential sensitivity of NSCLC cells to gefitinib could be attributed to the ability and inability of gefitinib to inhibit GLUT1 in each NSCLC cell. This evidence concerns the gene SLC2A1 and non-small cell lung carcinoma.