In ENKTL, macrophages recruited into the TME can be skewed toward an immunosuppressive phenotype (M2-like) and interact with tumor-infiltrating T cells through the expression of immune checkpoints, such as CD80/CD86-CTLA4, PD-L1/PD-L2-PD-1, and Galectin-9-TIM3 [52,53]. The gene discussed is CTLA4; the disease is neoplasm.