Our observation of elevated expression of embryotoxic cytokines TRAIL, and a trend towards increased IL1A, TNF and IFNG in hyperglycemic conditions, provides a direct mechanism contributing to the impact of diabetes on altered developmental trajectory of offspring, and support earlier reports of elevated uterine TNF and reduced TGFB2 and LIF accompanied by impaired blastocyst development in diabetic rat and mouse models39–41. The gene discussed is IL1A; the disease is diabetes mellitus.