To investigate whether accelerated diabetes development and enhanced islet infiltration in TLR4-deficient NOD mice is caused by an increased susceptibility of their pancreatic beta cells towards inflammatory mediators we exposed cultivated islet cells of TLR4+/+ and TLR4−/− mice to a mixture of TNFα, IL-1β and IFNγ or to the NO-donor DETA-NO (Figure 4). The gene discussed is IFNG; the disease is diabetes mellitus.