In conclusion, our results provide additional details to the role of TGF-β intracellular signalling pathway in OS and AD differentiation of hBMSC and identify SERPINB2 as a negative regulator of these effects Fig. 8D illustrates our current working model for the role of TGF-β on hBMSC through the suppression of SERPINB2 gene and we provide a possible list of down-stream targets ACTA2, TPM1, c-JUN, and JNK. Future studies are required to clarify the mechanistic role of SERPINB2 in vivo skeletal biology. This evidence concerns the gene TGFB1 and Alzheimer disease.