While it is not clear what leads to the nuclear accumulation of GSK-3β we have previously observed in human PDA (Ougolkov et al., 2006), our data shown here would suggest that nuclear GSK-3β (comparing NGC to KNGC mice) alone cannot promote progenitor ductal cell retention but requires the cooperation of KRasG12D signaling pathways that remain to be elucidated. Here, GSK3B is linked to Patent ductus arteriosus.