These findings collectively demonstrate that glycolytic enhancement in colorectal cancer is a tightly regulated metabolic adaptation driven by key oncogenic pathways (Wnt, KRAS, PI3K/AKT/mTOR), tumor suppressor dysfunction (p53) which together support malignancy by prioritizing glycolysis for energy, biosynthesis, and microenvironmental adaptation. The gene discussed is MTOR; the disease is colorectal cancer.