IL23A and myocardial infarction: Unexpectedly, Yan et al. also reported that IL-23 deficiency amplifies the inflammatory response and promotes the release of various inflammatory factors, especially IL-17, which further promotes the infiltration and deposition of γδT cells in the left ventricle, promotes the apoptosis of cardiomyocytes, and aggravates cardiac fibrosis in a murine myocardial infarction model (Yan et al., 2012).