Such findings include the loss of effector cell function and increased metastasis in response to STAT3 inhibition [3], type I IFN-driven STAT3-dependent induction of cytotoxicity in tumor-infiltrating T cells to suppress tumor formation [233], and IFNAR1:STAT1-dependent Treg expansion and the production of IL-10 in the TME [234]. The gene discussed is IFNAR1; the disease is neoplasm.