In vitro experiments showed that in the presence of Receptor Activator of Nuclear Factor-κ B Ligand (RANK-L) and macrophage colony-stimulating factor (M-CSF), DR3-dependent TL1A promoted osteoclast formation in RA patients and mice model, suggesting that TL1A drives the bone pathology of RA (64). This evidence concerns the gene CSF1 and rheumatoid arthritis.