,47 Should these results be replicated in future analyses that avoid weak instrument bias, this would fit with the “unopposed estrogen” hypothesis for the development of endometrial cancer, which postulates that endometrial cancer develops as a result of increased estrogen (which is influenced by insulin levels and is a direct product of the aromatization of testosterone) unopposed by SHBG.47 This evidence concerns the gene SHBG and endometrial cancer.