Caspase-1 activation, following further processing by precursor caspase-1, cleaves prointerleukin-1β (pro-IL-1β), pro-IL-18, and gasdermin D (GSDMD), consequently forming transmembrane pores with the N-terminus of the GSDMD (GSDMD-N) and facilitating the release of proinflammatory cytokines, such as IL-1β and IL-18, and the dysregulation of intracellular and extracellular ion gradients, exacerbating inflammation and ultimately triggering pyroptosis following viral infection [20,21]. This evidence concerns the gene CASP1 and viral infectious disease.