These data indicate that the Th1-related immune nature of the NOD genome facilitates the proliferation of the parasites in the absence of opn, at least in the early phases (Fig 4C), while in its presence (Fig 4A), these responses are likely moderated by the synergistic effects exerted on the opn by the infection and the autoimmune-prone genetic setting in relation to the Th1/Th2 balance. The gene discussed is SPP1; the disease is infection.