IL−4/STAT6 signaling is a central driver of M2-like phenotypes: IL−4 binding to its receptor activates Janus kinases (JAKs), which phosphorylate STAT6, enabling STAT6 to translocate into the nucleus and induce transcription of anti-inflammatory and pro-tumor genes such as Arg1, MRC1 (CD206), and CCL18. The gene discussed is MRC1; the disease is neoplasm.