IL17A and myocardial infarction: Inflammation and immune responses play a crucial role in the pathogenesis of post‐MI remodeling.1, 2, 3 It has been reported that toll‐like receptor 4 mediates maladaptive left ventricular (LV) remodeling and impairs cardiac function after MI.4 Moreover, experimental studies from our laboratory demonstrated that interleukin (IL)–17A promotes ventricular remodeling after MI.5 These findings suggest that excessive immune‐mediated inflammatory reactions play a deleterious role in postinfarction ventricular remodeling.