Research on pyroptosis began in 1986 when Friedlander observed that anthrax lethal toxin (LT) treatment of primary mouse macrophages led to cell death and rapid release of cell contents. In 1989, Cerretti et al. and Thornberry et al. identified ICE (interleukin-1β-converting enzyme, caspase-1) as an inflammatory caspase. Zychlinsky et al. made the first observation of pyroptosis in 1992, noting its occurrence in Gram-negative bacterial pathogen Shigella-infected macrophages. Chen and colleagues (1996) discovered that Shigella flexneri invasion plasmid antigen B (ipaB) directly attaches to ICE, activating the enzyme within infected macrophages. Initially mistaken for apoptosis due to similarities such as caspase dependence, DNA damage, and nuclear condensation, this form of cell death was later recognized as distinct. The term ‘pyroptosis,’ derived from the Greek word’s ‘pyro’ (fire/fever) and ‘ptosis’ (falling), was coined to describe pro-inflammatory programmed cell death (D’Souza and Heitman, 2001).