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. The gene discussed is STK11; the disease is AIDS dementia complex.