After ischaemic stroke, DAMPs released by necrotic cells in the ischaemic core and changes in intracellular microenvironment can trigger the formation of inflammasomes complexes, activating caspase-1 and mediating the secretion of IL-1β and IL-18, and finally cause cell death through inflammation and/or apoptosis. This evidence concerns the gene CASP1 and ischemic stroke.