NLRP3 is an important component of the inflammatory response that is activated by damage-associated molecular patterns (DAMPs), such as reactive oxygen species (ROS), K+, Ca2+, and acids released by damaged tissues after stroke [14], and subsequently mediates caspase-1 activation to cleave and produce mature IL-1β and IL-18, ultimately leading to neuroinflammation or pyroptosis [15]. Here, IL1B is linked to stroke disorder.