Characteristic pathologies of osteoarthritis joints, such as cartilage injury, osteophyte formation, and synovial fibrosis, appear to be caused even by high levels of active TGFβ and altered signaling pathways in chondrocytes [21, 22], while Smad3 is a key protein in the TGFβ pathway, and an assessment of the cogenetic etiology between osteoarthritis and bone density suggests that SMAD3 is a new osteoarthritis risk site [23, 24]. Here, SMAD3 is linked to osteoarthritis.