Among many stratagems employed by the bacterium to harm bone, Brucella can infect and survive within human and murine osteoblasts, and this infection triggers the secretion of receptor activator of nuclear factor-κB ligand (RANKL), proinflammatory cytokines, and chemokines that could be implicated in the presentation of osteoarticular brucellosis. This evidence concerns the gene TNFSF11 and infection.