Further analysis of primary mouse cardiomyocytes showed that cardiomyocyte-specific HSPB1 knockdown increased NF-κB activation, promoted the expression of proinflammatory mediators, increased leukocyte recruitment, and activated excessive inflammatory responses, ultimately leading to poor remodeling, cardiac dysfunction, and cardiac rupture after MI (51). The gene discussed is HSPB1; the disease is myocardial infarction.