Many studies have demonstrated that gene amplification, 3’UTR disruption, and the activation of signaling molecules, such as STAT1/3, NF-kB, and HIF1a, are involved in PD-L1 overexpression in tumor cells7; however, there have been fewer studies on the PD-L1 overexpression on TAMs than that on tumor cells. The gene discussed is STAT1; the disease is neoplasm.