Consistent with the role of the NLRP3 inflammasome as a mediator of inflammatory cell death following AMI, both genetic and pharmacological inhibition of its components (caspase 1, IL-1β, ASC, and NLRP3) have been demonstrated to reduce MI size (Coll et al., 2015; Kawaguchi et al., 2011; Marchetti et al., 2014; Mezzaroma et al., 2011; Pomerantz, Reznikov, Harken, & Dinarello, 2001; Sandanger et al., 2013). Here, NLRP3 is linked to myocardial infarction.