Present study showed that the relative expression of XIST was markedly raised in the I/R model group while decreased in the emodin group, and the overexpression of XIST reversed the protective effect of emodin on myocardial infarction, oxidative stress, and cardiomyocyte apoptosis, which is similar to the results studied by Wang et al. [25]. The gene discussed is XIST; the disease is myocardial infarction.