In pituitary tumorigenesis there is cross-talk between fine deregulation of intracellular pathways and complex microenvironmental factors, processes that can be modulated at various levels. The signaling pathways of growth, angiogenic factors and hormones are intricate; therefore, alterations induced upon node-molecules can lead to aberrant proliferation. The demonstrated overactivity of AKT and MAPK pathways qualifies them as valuable targets for inhibition mediated by somatostatin analogues. An increasing body of evidence suggests clinically significant implications of PTTG1 in correlation with aggressive phenotypes or survival rate, thus PTTG1 is an interesting candidate biomarker for malignancy, tumor staging and subsequent therapeutic interventions. Future work should focus on understanding the molecular mechanisms that control pituitary tumor transformation, where intracellular signaling molecules will constitute not only diagnostic/prognostic markers but also novel therapeutic targets.