The majority of TAMs display an M2-esque, anti-inflammatory phenotype, induced through IL-4, IL-13, and IL-10 signaling and, through the secretion of anti-inflammatory factors such as TGF-β and CCL22 (which recruits Tregs) and upregulation of immune checkpoints, inhibit anti-tumor T-cell responses [133,134] and promote many aspects of tumor biology, including migration and angiogenesis [135,136]. The gene discussed is IL4; the disease is neoplasm.