Inhibition of the IFN-γ function in non-obese diabetic (NOD) mice using either IFN-γ-specific antibodies42 or soluble IFN-γ receptors (IFN-γ-R)43 reduced the incidence of spontaneous diabetes and also prevented the transfer of diabetes via splenocytes from NOD donor mice44. Here, IFNG is linked to diabetes mellitus.