In summary, all these results suggest that in T1DM-prone NOD mice the insufficiency in IFN-γ/IDO1/AhR axis is present, thus any attempts to the reinforcement of this axis in appropriate cells of the immune system could be one of the ways of preventing T1DM in this model, through the restoration of the immunotolerance to pancreatic autoantigens. The gene discussed is IFNG; the disease is type 1 diabetes mellitus.