41 reported that in type 1 diabetes mellitus, activation of mTORC1/p70S6K enhanced oxidative stress, and subsequently induced podocyte apoptosis, whereas inhibition of mTORC1 decreased podocyte apoptosis, and attenuated mesangial expansion and albuminuria. The present data showed that exenatide administration reduced mTORC1/p70S6k phosphorylation in heart of diabetes mellitus rats. An in vitro experiment also showed that GLP‐1 treatment alleviated the high‐glucose‐induced increase in p‐mTOR expression and the decrease in p‐Raptor expression in cardiomyocytes. The gene discussed is RPTOR; the disease is diabetes mellitus.