However, peripheral TNFα and IL-1β do not explain, alone, the peripheral component of T. cruzi infection-induced pain because hyperalgesia started by the 2nd day, and the production of these cytokines peaked at the 14th day of infection without significant levels at the 7th day p.i. These results raise the possibility that other peripheral cytokines/molecules might also be involved in T. cruzi pain. The gene discussed is TNF; the disease is infection.