ZIKV infection upregulates transcription of IL-1β and IL-6 by activating NF-κB signaling, but does not trigger NLRP3-dependent ASC oligomerization and secretion of active caspase-1 and IL-1β even after LPS priming and ATP stimulation of macrophages and glial cells. ZIKV NS3 overexpression leads to the degradation of NLRP3 (probably, by its cleavage). NS1 and NS5 proteins do not have any impact on NLRP3 inflammasome. ZIKV infection influences only NLRP3-dependent but not AIM2-dependent caspase-1 activation and IL-1β secretion. The gene discussed is KRAS; the disease is Zika virus infectious disease.