Though both Cre “drivers” (i.e., Wnt1-Cre and P0-Cre) used to create Evc2/Limbin-cKO mice are expressed throughout the jaws and facial skeleton, Wnt1-Cre-based recombination efficiency in the anterior skull base is much higher (100% vs. 50% for Wnt1-Cre and P0-Cre, respectively), results in worse midfacial deficiency, and causes greater skull base defects that in their Evc2/Limbin-P0-cKO counterparts [53]. This evidence concerns the gene EVC2 and hyperinsulinemic hypoglycemia, familial, 4.