Moreover, STAT3 inhibition most likely does not exert antineoplastic effects by purely cell-autonomous mechanisms [41] as its blockade is expected to limit the production of pro-inflammatory factors, hence reducing local inflammatory reactions, and stimulate the recruitment of immune effectors into the tumor bed and improve immunosurveillance, especially in the context of ongoing anticancer immune responses [42]. This evidence concerns the gene STAT3 and neoplasm.