STAT is an interferon-inducible product, and the activation of STAT1 in tumor-associated MΦ (TAMs) can lead to the upregulation of both inducible nitric oxide synthase (iNOS) and Arginase I. These enzymes play significant roles in suppressing T cell function—iNOS by generating nitric oxide, which can directly inhibit T cell activity (70), and Arginase I by depleting L-arginine, an amino acid essential for T cell proliferation and function (71). This evidence concerns the gene STAT1 and neoplasm.