Moreover, in numerous cancer types, mTOR is overexpressed as a result of genetic changes or abnormal activation of PI3K/AKT pathway elements, leading to disruptions in cell proliferation, differentiation, growth, and viability. Zhang and colleagues reported that exenatide inhibits EC cell growth by suppressing phosphorylation, leading to the inhibition of mTOR phosphorylation and promotion of apoptosis. This evidence concerns the gene AKT1 and cancer.