Consistent with this notion, recent studies have demonstrated a specific inhibitory role for Dll4 in the recruitment of HE to nascent hematopoietic clusters forming in the AGM (Porcheri et al., 2020), presumably by sustaining high Notch signal activity in HE, thus maintaining the expression of arterial genes such as Hey1 and Hey2 and preventing the endothelial to hematopoietic transition. This evidence concerns the gene HEY1 and hereditary elliptocytosis.