Considering the recently described plasticity of NSCLC and potential for ADC to escape treatment through LKB1 inactivation or dysregulated pentose phosphate pathway-mediated metabolic reprogramming and squamous transdifferentiation in KL mice52, our characterization of GLUT1-mediated glycolytic metabolism in SqCC may be an important step in identifying and preventing potential mechanisms of acquired resistance in ADC. Here, SLC2A1 is linked to non-small cell lung carcinoma.