Recent studies demonstrate that an overexpression of B-Raf mRNA and protein is a feature of nonfunctional pituitary adenomas; that overactivity highlights an overactivity of the Ras-B-Raf-MAP kinase pathway to promote pituitary tumorigenesis [82], and that the low levels of Raf kinase inhibitory protein (RKIP) in a GH-pituitary adenoma correlate with poor clinical response to somatostatin analog therapy because RKIP can bind to and inhibit Raf1 kinase to attenuate MAPK signaling [83]. This evidence concerns the gene TGM2 and pituitary gland adenoma.