In addition, Lin et al. also observed the overexpression of the lncRNA XIST in the infarct area and showed that the lncRNA XIST accelerated myocardial apoptosis after MI by targeting miR-101A-3p to upregulate FOS and apoptosis-related protein expression in a mouse model of MI [59]. The gene discussed is FOS; the disease is myocardial infarction.