Indeed, we found that E13 fetal liver HSCs with the deletion of Jarid2 expression from Vav1Cre + /−Jarid2fl/fl mice have activated the Mef2/PGC1a pathway and induced fasting hyperglycemia, impaired glucose tolerance, and IR in wild-type recipients of VD(+) Jarid2−/− HSCs when compared to recipients of fetal liver Jarid2 + /+ HSC, confirming the importance of the downregulation of HSC Jarid2 in programming immune cells to cause IR (Fig. 3C–E). This evidence concerns the gene JARID2 and Hyperglycemia.