These findings suggest that MEK inhibition does not only contribute to creating MDSC-hostile conditions in the TME by attenuating the expression of immunosuppressive factors by tumor and stromal cells but might also directly influence intracellular, RAS-RAF-MEK-ERK-dependent proliferative and prosurvival processes in MDSCs, leading to an overall increased protective anti-tumor immune response (12, 208). This evidence concerns the gene MAPK1 and neoplasm.