Pituitary adenomas originate only in the anterior lobe. In the vast majority of cases, they are monoclonal and are characterised by complete disruption of the reticulin fibre network in contrast to pituitary hyperplasia1. These adenomas are benign lesions, comprising 10-15% of all intracranial tumours2,3. Pituitary adenomas can be divided in secreting and non-secreting tumours. Secreting tumours produce an excess of pituitary hormones with each its own syndrome: Pr (Prolactinoma), GH (Acromegaly, gigantism), ACTH (Cushing’s disease), TSH (Thyrotrophinoma), and LH/FSH (Gonadotrophinoma). Although almost all pituitary adenomas are classified as benign, many of these lesions are locally invasive and cause major morbidity and mortality. The pathogenetic mechanism in pituitary tumour genesis is complex and enigmatic4.