The tumor microenvironment (TME) is characterized by hypoxia and the production of reactive molecules.[12] Exogenous nitric oxide (NO), which is derived from multiple cellular sources including tumor cells, tumor‐associated monocytes (TAMos), tumor‐associated macrophages (TAMs), or fibroblasts, can impede T cell proliferation or precipitate the anergy and apoptosis of T cells.[13] The targeting of nitric oxide synthase (NOS) has garnered considerable interest in clinical trials as a potential cancer treatment. The gene discussed is NOS2; the disease is cancer.