The first function is to sense cytosolic viral infection and activate NF-κB via MAVS and a complex of the adaptor CARD9 and Bcl-10, resulting pro-IL-1β production; the second function is to bind ASC and thereby trigger caspase-1-dependent inflammasome activation and IL-1β generation via a NLRP3-independent mechanism [61, 63]. This evidence concerns the gene NLRP3 and viral infectious disease.