In line with our previous findings regarding the function of mammalian CT as a physiological inhibitor of bone formation (Keller et al., 2014), we found the expression of the key osteoblast transcription factor Runx2 to be significantly enhanced in Calcr−/− CAIA mice, accompanied by increased expression levels of osteoclast markers Acp5 and Ctsk. This indicates that during RA, the CTR is required to limit excessive bone turnover as a whole, rather than bone formation or resorption singularly. Here, CALCR is linked to rheumatoid arthritis.