Several chemokine ligands and interleukin (IL)-1-beta (drivers of chemotaxis) and innate immunity-related terms were enriched only in TIM-3 increase patients, reflecting an inflamed tumor microenvironment.30 Meanwhile, acute inflammatory response genes SAA1 and ORM1/2 and metabolic enzymes PHGDH and SHMT1/2, which drive essential metabolite biosynthesis for effector T-cell expansion,31 were among the leading edge genes in TIM-3 decrease patients. The gene discussed is HAVCR2; the disease is neoplasm.