The infection is characterized by two stages; during the early stage there is a strong inflammatory immune response mediated by T cells and involving classically IFN-γ-activated myeloid cells (so-called M1) required for the efficient control of the first most prominent parasitemia peak through their production of trypanotoxic molecules, such as nitric oxide (NO) and Tumor Necrosis Factor (TNF), and the phagocytosis of antibody-opsonized parasites that occurs mainly in the liver [8–12]. This evidence concerns the gene IFNG and infection.