Both the inhibition of AIM2 and NLRP3 prevented inflammasome activation in the CCA plaque after stroke, with greater efficacy of the AIM2 inhibitor, whereas only the AIM2 inhibitor significantly prevented the post-stroke increase in IL-1β levels in the CCA plaque (Fig. 2f,g and Extended Data Fig. 6c). Here, AIM2 is linked to stroke disorder.