To date, several NLRP3 inflammasome activation pathways have been established: the canonical pathway which comprises of a two-signal model involving priming (signal 1) and activation (signal 2); a non-canonical pathway that necessitates caspase-4/caspase-5, secretion of IL-1β and IL-18 which respond to a particular intracellular lipopolysaccharide (LPS)-induced infection of gram-negative bacteria; and the alternative pathway driven by toll-like receptor 2 (TLR2) or TLR4 signaling without implicating additional secondary activators [35,36,37]. This evidence concerns the gene TLR2 and infection.