The decrease in PAX6 may explain the presence of diabetes, although HNF1B does not bind PAX6 directly.36 Another model for HNF1B−/+ showed an impaired β cell differentiation and reduced proliferation of the foregut and pancreatic progenitors, which addressed the underlying cause for pancreatic hypoplasia.37 The HNF1B−/+ pancreatic progenitors, compared to their isogenic controls, also showed decreased expression of HNF1A and the Hippo signaling regulator, ROBO2, the downstream targets of HNF1B.37 Here, PAX6 is linked to diabetes mellitus.