IFN-γ and TNF-α, which are abundantly produced in Chagas disease in response to the perennial stimulus of T. cruzi [2,21,22], cause a reduction in oxidative metabolism, in the expression of energy metabolism enzymes, in the activity of lipid beta-oxidation and in the production of mitochondrial ATP, and reduction in the action of mitochondrial membrane potential (ΔΨm) via the NF-κB-dependent signaling pathway [3,23,24,25,26,27,28,29]. This evidence concerns the gene IFNG and Chagas disease.