Moreover, tumor-associated macrophages (TAMs) including M2-like macrophages (or alternatively activated macrophages) promote fibrosis and inhibit both adaptive and innate antitumor immunity by secreting immunosuppressive molecules including transforming growth factor–β (TGF-β), interleukin-10 (IL-10), and arginase 1 (Arg1), thus negatively affecting patient outcomes (4, 5). Here, ARG1 is linked to neoplasm.