This cell-specific high-expression pattern suggests that TKT may act as a key molecule linking the abnormal proliferation of CRC epithelial cells and the macrophage-mediated inflammatory response in AS by regulating tumor cell metabolism and immune cell function respectively, further supporting the core role of the “cell cycle-lipid metabolism-immunity” crosstalk regulatory network in the comorbidity mechanism of the two diseases. The gene discussed is TKT; the disease is neoplasm.