Using both in vitro and in vivo models with the tetracycline-controlled expression of mutant KRAS, studies have shown that oncogenic KRAS promoted glucose uptake, pentose phosphate pathway (PPP), hexosamine biosynthesis pathway, and the metabolic switch from oxidative phosphorylation to glycolysis, in order to provide building blocks for cancer cell survival and proliferation [16,17]. The gene discussed is KRAS; the disease is cancer.