ATOH8 transcriptionally activated HK2-mediated glycolysis and inhibited cell death pathway in CTCs, thus mediating the intravascular survival of colorectal tumor cells in the circulation, and ultimately providing a novel potential target for the prevention and treatment of hematogenous metastasis in CRC (166, 174) Metabolism and cell survival are inextricably linked, and cancer cells can switch between different metabolic states to respond to adverse conditions such as metabolic stress, anoikis, and mechanical stress (131, 175). This evidence concerns the gene ATOH8 and colorectal carcinoma.