This inflammatory activity constitutes a critical aspect of the pathophysiological mechanism in cardiac ischemia, involving various regulatory elements, including interleukin-1 beta (IL-1β) [11] and the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome complex [12], which serves as a principal mediator of sterile inflammation post-acute myocardial infarction [13]. Here, IL1B is linked to myocardial infarction.