In pancreatic ductal adenocarcinoma, KRAS facilitates ribose biosynthesis by diverting intermediate glycolytic metabolites into the non-oxidizing arms of the pentose phosphate pathway [158], and the expression of GLUT1 and glucose uptake in CRC are mainly dependent on KRAS duplication mutations, which allow KRAS-driven CRC cells to survive in a low-glycemic environment for long periods of time [159,160]. This evidence concerns the gene KRAS and colorectal carcinoma.