There is an example: EndMT plays an important role in pathophysiological processes such as myocardial ischemia-reperfusion, myocardial infarction, diabetic cardiomyopathy, and fibrosis; and TGF-β-induced EndMT can be attenuated by knocking down the LINC00961 by a mechanism related to activation of phosphatase and tensin homolog (PTEN) expression and inhibition of PI3K, AKT, and mammalian target of rapamycin (mTOR) (Hu et al., 2022). This evidence concerns the gene PTEN and myocardial infarction.