Nevertheless, in the present study, HSD17β1 did not cause endometrial carcinoma, suggesting that other mechanisms, such as inactivation of phosphatase and tensin homolog, loss of forkhead box O subclass transcription factor 1, and hyperactivity of the phosphoinositide-3 kinase pathway, play crucial roles in the development of endometrial cancer [24]. This evidence concerns the gene HSD17B1 and endometrial cancer.