Since IL-1-induced beta cell apoptosis is potentiated by other proinflammatory cytokines, such as TNFα, IFNɣ, and IL-6, and since anti-TNF therapy improved beta cell function in a small placebo-controlled trial [7], it is likely that a combination of treatments targeting various aspects of signaling caused by the cytokine network is needed to improve the efficacy of anti-cytokine strategies in T1D, as has indeed been demonstrated in animal models [8]. The gene discussed is TNF; the disease is type 1 diabetes mellitus.