Interleukin-4 (IL-4) can bind to type I IL-4R intracellularly to activate the JAK1-STAT6 pathway inducing M2 polarization of TAMs (Roskoski, 2016), upregulating checkpoint molecules (such as PD-L1), and recruiting regulatory T cells, thereby synergistically promoting tumor immune escape (Jiménez-Garcia et al., 2015). The gene discussed is JAK1; the disease is neoplasm.