Results from preclinical studies indicate that EGFR mutations or KAS mutations cause activation of the EGFR/KRAS/MEK/ERK signaling pathway,[384, 385, 386] which subsequently regulates the expression of C‐MYC and increases the expression levels of GLUT1 and HK2 genes.[387] This may eventually lead to an increase in the glycolytic flux of tumor cells. The gene discussed is EGFR; the disease is neoplasm.