Indeed, HMGA1 is able to inhibit the proapoptotic activity of p53 in thyroid cancer cells [18] while both HMGA1 and HMGA2 can enhance transcription factor E2F1 (E2F-1) activity displacing histone deacetylase 1 (HDAC1) from retinoblastoma-associated protein (pRb) and enhancing E2F-1 activity thus overcoming pRb mediated G0 arrest and promoting the development of pituitary adenomas [19,20]. This evidence concerns the gene HDAC1 and pituitary gland adenoma.