MDSCs mainly inhibit T cell function by producing arginase I (Arg1), reactive oxygen species (ROS), and immunosuppressive cytokines such as IL-10 and TGFβ through activating STAT3, C/EBPβ, PI3K, and MAPK signaling pathways [24–29], which skews MDSCs into M2-like tumor-promoting phenotype [30, 31]. The gene discussed is ARG1; the disease is neoplasm.