APC and chronic primary adrenal insufficiency: If the stabilization of CTNNB1 at an early time point of adrenal development (either by inactivating Apc or by expressing a constitutively active form of CTNNB1 that lack the phosphorylation sites on exon 3 necessary for its degradation) led to significant adrenal hypoplasia during development [15,17], its stabilization at later time points (either by inactivating Apc with a less efficient Nr5a1-cre [15] or by expressing the Ctnnb1ex3 allele in Akr1b7+ cells [46]) rather led to an increase in cellular proliferation and adrenal dysplasia.