Leptin-treated female NOD mice exhibited accelerated type 1 diabetes onset and mortality, along with enhanced Th1 responses, evidenced by abundant IFN-γ mRNA-expressing cells in splenic periarteriolar sheaths despite no significant change in overall IFN-γ or IL-4 secretion from stimulated splenic T cells compared to controls [175]. The gene discussed is IFNG; the disease is type 1 diabetes mellitus.