Th1 differentiated effector BDC2.5 CD4+ T cells cause diabetes after transfer into wildtype NOD mice in a process heavily dependent on production of IFN-γ (Fig 4A) [30], and we hypothesised that administration of IC87114 via oral gavage which can stop IFN-γ production from these cells in vitro, would inhibit or delay onset of diabetes in the IFN-γ dependent model of disease. The gene discussed is CD4; the disease is diabetes mellitus.