Considering the rapid activation of NLRP3 inflammasomes by IRAK1, and the important role of NLRP3 inflammasomes in the pathogenesis of EAE, we speculate that IRAK-M may suppress the activation of NLRP3 inflammasomes and pyroptosis in microglia and subsequently attenuate the onset of MS/EAE in an IRAK1-dependent manner. This evidence concerns the gene IRAK1 and myeloid sarcoma.