After a functional confirmation of osteoclastogenic potential for CD3−CD19−CD56−CD11b+CD14+ cells, but without increases in the number of differentiated TRAP+ OCs under M-CSF/RANKL stimulation in patients with arthritis, we hypothesized that the enhanced OCP activity might be caused by the complementary proinflammatory/osteoclastogenic stimuli, namely chemokine signals [3]. This evidence concerns the gene CSF1 and arthritic joint disease.