AKT1 and endometrial cancer: Studies have shown that after estrogen acts on human endometrial cells, the phosphorylation of PI3K is significantly increased, thereby inhibiting the apoptosis of endometrial cells, but the use of estrogen nuclear receptor antagonists cannot prevent this response, which indicates that as a causative agent, excessive or unopposed estrogen can activate the PI3K/AKT signal transduction pathway in endometrial cancer cells through non-transcriptional effects to promote cell proliferation (Qu et al., 2015).