These data suggest that the overactivation of noncanonical TGFβ/ALK5/AKT signalling and the subsequent up-regulation in CCK1R, not only makes Lrg1-/- mice more susceptible to caerulein-induced acinar cell injury but also explains the increased pancreatic regeneration following the AP in the absence of Lrg1. Here, AKT1 is linked to alkaline phosphatase measurement.