As reported by other authors in similar models in which arthritis or experimental autoimmune encephalomyelitis (EAE) is induced in mice deficient in EphA4 [21], or in ephrin-B1, ephrin-B2 or ephrin-B1/B2, main ligands of EphB2 and EphB3 [19, 22, 43], the immune response was remarkably low in both EphB2- and EphB3-deficient mice resulting in a low incidence of disease, and was totally null in EphB2−/− mice. This evidence concerns the gene EPHB2 and arthritic joint disease.