Epidemiological studies suggest that CCR5-Δ32 variant is associated with a reduced incidence and severity of bone destruction disease such as rheumatoid arthritis.84 Inhibition of Ccr5 in mice decreased osteoclast formation suggesting beneficial skeletal effects of the functional loss of Ccr5.85,86 Blocking of CCR5 using antibodies impaired human osteoclast function in vitro.87Ccr5 deficient (Ccr5−/−) mice were less susceptibility to osteoporotic stimulation via the administration of RANKL, which induces osteoporosis. The gene discussed is CCR5; the disease is osteoporosis.