From the observed Th1 response, mainly upregulation of interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα) occurring during the mid and late infection phases, led to severe mitochondrial dysfunction involving loss of complex-I and IV quantity and activity accompanied by a reduction in mitochondrial phosphorylation capacity, membrane potential and mitochondrial ATP generation [14]. The gene discussed is IFNG; the disease is infection.