However, forced expression of jag1a in the endothelium of tgfbR2 morphants rescued the loss of runx1 and cmyb expression (Figures 6D and 6E), confirming that the hematopoietic defects in tgfbR2 morphants are mainly due to loss of jag1a. We conclude that autocrine TGFβ1 and paracrine TGFβ3 signal to the endothelium through TgfβR2, inducing jag1a expression, which in turn induces HE programming and HSPC emergence. Here, TGFBR2 is linked to hereditary elliptocytosis.