As expected, CFA-induced joint inflammation leads to bone loss, which has also been reported in animal models of joint inflammation.3 This is also common in human conditions with chronic joint inflammation, such as rheumatoid arthritis.43,46 In pathological conditions, overexpression of certain molecules, such as IL-6, TNF, histamine, and NGF, in the joints can promote osteoclast overactivity and diminished osteoblast activity. The gene discussed is TNF; the disease is rheumatoid arthritis.