An indirect support to the role played by IL-1β—a prototypical NLRP3 inflammasome activation-derived cytokine—in the pathogenesis of MS stems from the observation that successful treatment of disease relapses in MS patients with glatiramer acetate or IFNβ results in the increase of endogenous IL-1Ra concentration [56,57]. This evidence concerns the gene IFNB1 and myeloid sarcoma.