Juvenile DM (JDM), characterized by substantial increases in type I interferon (IFN) and immature transitional B cells, provides evidence for the involvement of B cells in the etiology of IIM.17 Furthermore, the serum and muscle fibers of IIM have higher levels of B cell activating factor, a member of the tumor necrosis factor (TNF) family.18 These findings support the hypothesis that B-cell depletion may reduce the severity of IIM and have a beneficial effect on its disease burden. The gene discussed is TNF; the disease is dermatomyositis.