PTGS2 and Miyoshi myopathy: Aiming to implement MDSC-dependent immunosuppression halting strategies, several attempts have been made to interfere with cyclooxygenase-2 (COX-2), arginase-1 expression, and inducible nitric oxide synthases and to decrease reactive oxygen species production and provided undeniable rational for the novel association of anti-inflammatory compound to the MM therapeutic backbone, in order to expand the effectiveness of immunotherapy and to decrease the myeloid-derived population in the MM environment [118].