Increased formation of osteoclasts was shown for cultures of peripheral blood mononuclear cells from RA patients associated with enhanced myelopoiesis [29] but Li and co-workers [30] demonstrated, using a human TNF-transgenic mice arthritis model, that enhanced osteoclast formation was confined to precursor cells isolated from blood and spleen and that osteoclastogenic potential of bone marrow precursors remained unaffected. The gene discussed is TNF; the disease is rheumatoid arthritis.