PDE11A and ACTH-independent Cushing syndrome: Activating mutations in the stimulatory G-protein alpha subunit (GNAS) and the catalytic subunit of PKA (PRKACA), as well as inactivating mutations in the type 1 alpha regulatory subunit of PKA (PRKAR1A) and cAMP-hydrolyzing PDEs (PDE11A and PDE8B), have been linked with various morphological correlates of ACTH-independent adrenal Cushing syndrome (6, 36, 63, 64).