Gr1+ CD11b+ F4/80− MDSCs can be further divided into Ly6C+ monocytic and Ly6G+ granulocytic populations and depending on their contextual expression (e.g., tumor microenvironment, site of chronic inflammation) each can evoke immunosuppression via arginase I (Arg I) and inducible nitric oxide synthase (iNOS), thus inhibiting T cell activation [28, 29]. The gene discussed is ITGAM; the disease is neoplasm.