Third, RA patients have higher articular TNF levels than patients with less destructive forms of arthritis [30] and osteoclastogenesis requires higher amounts of TNF than synovial inflammation [21]; thus, incomplete TNF inhibition will reduce bioactive TNF levels below the threshold of osteoclastogenesis stimulation, even if leaving sufficient TNF to continue eliciting inflammation [31]. The gene discussed is TNF; the disease is arthritic joint disease.