Specifically, selumetinib reduced populations of CD11b+ Ly6G+ tumor-infiltrating neutrophils or gMDSC, blocked monocytes from differentiating into TAMs at the Ly6C+MHCII+ intermediate state within the tumor bed [22, 23], and concomitantly inhibited the expression of Cox-2 and Arg-1 – both of which are considered to be key mediators of immunosuppressive pathways [26, 27]. Here, PTGS2 is linked to neoplasm.