In fact, subclinical infection is the result of an effective T helper 1 (Th1) cellular immunity, with the activation of macrophages by interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) and the elimination of intracellular amastigotes via the l-arginine nitric oxide pathway [2, 3]. This evidence concerns the gene IFNG and infection.