To demonstrate phosphorylation-mediated inactivation of BAD contributes to the development of experimental arthritis, we performed CIA in Bad3SA/3SA knockin mice, in which the regulatory serine sites were mutated to alanines so that the resultant BAD mutant can no longer be phosphorylated and inactivated (Datta et al., 2002; Figure 7A,B). The gene discussed is BAD; the disease is arthritic joint disease.