Among the elevated cytokines in patients with CADASIL, the increase of IL-1β is the most prominent, which has been appreciated as the leading factor in the NLRP3 inflammasome activation [74], as evidenced by the absence of caspase-8 compromised the consistent accumulation of pro-IL-1β and NLRP3 protein in the macrophages [75, 76]. Here, IL1B is linked to CADASIL.