Pattern recognition receptor (PRRs) signalling via MYD88 can induce activation of MAPKs and NF-κB, which up-regulate the transcription of genes including those encoding pro-IL-1β and NLRP3. A variety of stimuli trigger the formation of the various inflammasome complexes. Inflammasome assembly leads to the autoproteolytic cleavage and activation of caspase-1, which then cleaves a variety of substrates including pro-IL-1β and pro-IL-18, and the pyroptotic effector GSDMD. Cleaved GSDMD binds to lipids in the plasma membrane and forms oligomeric pores, enabling the release of IL-1β and IL-18. Pore formation also results in cellular swelling due to osmotic pressure and to the death of the cell. Plasma membrane rupture will typically follow pore formation however this is not a passive process due to osmotic swelling as long thought but is instead mediated by Ninj1 following osmotic swelling. Membrane rupture results in the release of cell contents too large to fit through the GSDMD pore. Inflammasome-independent pyroptosis occurs when caspase-4 or caspase-5 (caspase-11 in mice) directly binds LPS and triggers self-oligomerisation, activation of the caspases and cleavage of GSDMD. Unlike caspase-1 these caspases do not directly cleave pro-IL1β and pro-IL18.