The data indicated that BRAF inhibition resulted in the suppression of metabolites in TCA cycle (Supplementary Fig. S4A–G), confirming that series of our experiments demonstrated the concept that mutant KRAS status does not predict glucose dependence in culture, and that glutamine fuels oxidative phosphorylation in TCA cycle, as observed in a stress condition such as BRAF specific inhibition in colorectal cancer cells. This evidence concerns the gene KRAS and colorectal cancer.