Taken together with the highly conserved C-terminus of AIP, and specific mutations that occur on the Cα-7h, our results support the idea that this helix is involved in client protein interactions, at least with AhR and PDE4A5, and that loss of such interactions leads to a variety of biochemical changes in pituitary cells that predisposes to pituitary adenoma. This evidence concerns the gene AHR and pituitary gland adenoma.