To conclude, our results suggest that in Alk5/Wnt1-Cre mutants a noticeable increase in apoptosis coincides with the abnormal patterning of the PAAs and the aortic sac, and with the failed AP-septation. These data support a specific role for ALK5 signaling, either directly or indirectly, in CNCC survival, since a similar apoptosis of NC-derived cells is not seen in Tgfbr2/Wnt1-Cre mutants [8,9].