As an extensive inflammatory complex, the activation of the NLRP3 inflammasome elicits caspase-1 autocatalytic activation and subsequently facilitates the maturation and rapid secretion of proinflammatory cytokines, such as IL-1β and IL-18, which trigger a cascade of inflammatory responses through various pathways, including the nuclear factor kappa-B (NF-κB), activator protein 1, and c-Jun N-terminal kinase (JNK) [27, 28], and finally exacerbates EAE through robust recruitment of immune cells in the white matter of MS patients, increasing neurological disability [18, 29–31]. The gene discussed is NLRP3; the disease is myeloid sarcoma.