The best-characterized mechanism for this in CD is increased CDKN1B phosphorylation by cyclin E (upregulated in corticotropinomas), which inactivates the protein and triggers its degradation, although 14-3-3 and AKT-mediated phosphorylation have the same effect (Korbonits et al. 2002, Susaki & Nakayama 2007, Roussel-Gervais et al. 2010). The gene discussed is AKT1; the disease is ACTH-producing pituitary gland adenoma.