These inflammasomes are expressed in microglia, astrocytes, neurons, and endothelial cells depending on the pathophysiological conditions in stroke.[29] From 2008 to 2020, a growing body of evidence has suggested that activation of inflammasomes triggers neuroinflammation through caspase-1 that further activates various downstream events (e.g. IL-1β, IL-18, IL-6 or TNF-α) and contributes to cell death. This evidence concerns the gene IL18 and stroke disorder.