For instance, in cardiac fibrosis, it inhibits NAT10-mediated BCL-XL mRNA stabilization to reduce collagen deposition post-myocardial infarction [167]; in vascular remodeling, it suppresses ITGB1-FAK signaling to attenuate neointima formation [168]; and in inflammatory bone loss, it destabilizes Fos mRNA to block osteoclastogenesis [92]. This evidence concerns the gene NAT10 and myocardial infarction.