ZIKV infection activates NLRP3 inflammasome, and NS1 protein facilitates inflammasome assembly, by recruiting host deubiquitinase USP8 to cleave K11-linked polyubiquitin chains from caspase-1 at Lys134. This inhibits the proteasomal degradation of caspase-1 and stabilizes caspase-1, which promotes both IL-1β release and the cleavage of cGAS. The enhanced cleavage of cGAS leads to the decrease in recognition of mitochondrial DNA release and thus inhibits type I IFN signaling, as shown for THP-1, PBMC, and mouse brain tissues. The gene discussed is CGAS; the disease is Zika virus infectious disease.