MTOR and myocardial infarction: 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).