As with analyses of overall endometrial cancer, the effect of fasting insulin on endometrioid endometrial cancer attenuated toward the null when fasting insulin and bioavailable testosterone were combined into a single model (OR per increase in natural log transformed pmol/L fasting insulin 1.05, 95% CI 0.36 to 3.03, P = 9.33 × 10−1), potentially reflecting mediation via bioavailable testosterone or persistent weak instrument bias in this model. The gene discussed is INS; the disease is endometrial cancer.