For example, it has been described that B cells are enriched in the bone marrow and inhibits osteoblasts via the release of CCL3 and TNF [12], but also the abnormal activity of Wnt signaling, the receptor activator of nuclear factor-κB ligand (RANKL)-osteoprotegerin (OPG) signaling, as well as the bone morphogenetic proteins (BMPs) pathway and other mechanisms have been described to be altered in osteoblasts in rheumatic diseases [13]. Here, TNFRSF11B is linked to rheumatic disorder.