The immune escape mechanisms mediated by MDSCs also include nitrating lymphocyte-specific protein tyrosine kinase (LCK) inhibiting T cell activation (86), inducing T cell dysfunction through arginase 1 (Arg1) metabolism depletion of arginine (87), and tumor-derived extracellular vesicles (EVs) inducing MDSCs production, recruitment and activation (88). The gene discussed is ARG1; the disease is neoplasm.