Jag1a then activates the Notch receptor, presumably Notch1a (Espin-Palazon et al., 2014), and the signal-receiving cell becomes hemogenic by expressing specific markers such as gata2b, runx1, and gfi1aa. Loss of TGFβ signaling would therefore prevent HE from being specified by the Jag1a/Notch1a interaction. Here, RUNX1 is linked to hereditary elliptocytosis.