Our results show that arthritis pathogenesis was exacerbated in Bad−/− mice in both CIA and TNF-Tg murine models of RA, but protected in Bad3SA/3SA mice in CIA model, due to reduced or augmented apoptosis in synovial sublining macrophages, thereby adding BAD to the list of the key players that determine the susceptibility of mice to experimental arthritis. This evidence concerns the gene TNF and rheumatoid arthritis.