Khaiboullina et al. and Wang et al. demonstrated that ZIKV infection in monocyte-derived cells was associated with prolonged activation of NLRP3 inflammasome, as shown by the increased levels of IL-1β and caspase-1 secretion, and Zheng et al. associated ZIKV-induced inflammasome activation with the evasion of type I IFN-mediated host immune response [53,54,55]. The gene discussed is CASP1; the disease is Zika virus infectious disease.