They revealed not only “usual suspects” in the pathogenesis such as upregulation of inflammatory activator (TNFα, TGFB1, and LPS), transcriptional regulators (Fos, Nfatc1), and signaling proteins (Nfκb, Erk1/2, P38 Mapk, Src, P13k, Akt) that are known to promote osteoclast differentiation and bone resorption but also provided a number of new targets and novel insight into the role of Nampt in the pathogenesis of arthritis. This evidence concerns the gene TGFB1 and arthritic joint disease.