Transforming growth factor beta s (TGF beta s) were originally discovered due to their ability to promote anchorage-independent growth of rat NRK fibroblasts in the presence of TGF beta. TGF beta 1, TGF beta 2 and TGF beta 3 are each synthesized as precursor proteins that are very similar in that each is cleaved to yield a 112 amino acid polypeptide that remains associated with the latent portion of the molecules. TGF beta 3 mediates many intercellular interactions that occur during embryonic development, cell differentiation and epithelial homeostasis. TGF beta 3 overexpresses in extramammary Paget’s disease (EPD) and downregulates in Bowen’s disease, indicating that its expression is a useful indicator of tumor activity. TGF beta 3 levels strongly correlate with IGF-1 and osteocalcin levels in serum. Significant amounts of TGF beta 3 circulation appear to be representative of TGF beta 3 expression in bone and may in part be derived from bone. Glucocorticoids may block TGF beta production by modulating mRNA levels and c-Jun activity.