The processes of cell proliferation and related metastasis in COAD patients are very complex and mainly include the activation of oncogenes and the loss of function of tumor suppressor genes, leading to overactivation of signal transduction networks, including the TGF-β, Wnt/β-catenin, Smad, Notch, Hippo-YAP, MAPK, HIF-1, mTOR, and PI3K/Akt pathways, to promote cancer cell proliferation and metastasis [8,9,10,11,12,13,14,15,16]. This evidence concerns the gene MTOR and neoplasm.