As the major product of NLRP3‐mediated inflammation, IL‐1β promotes the recruitment and retention of macrophages during inflammatory conditions.[35] In agreement with our observations, a previous study showed MCC950 decreased infiltrating CD68+ macrophages in a mouse model of myocardial infarction and suggested IL‐1β suppression was, at least in part, a driving factor.[13] However, contrary to previous in vitro findings, MCC950 also reduced TNF‐α. Here, NLRP3 is linked to myocardial infarction.