Similarly, VIP alleviated the detrimental combined effect of infection, IFNγ and TNFα on mitochondrial membrane potential (10 nM: -57% to -21%, p<0.05; 0.5nM: -57% to -24%, p<0.05, Fig 3E) and revived the mitochondrial ATP generation from -60% to -20% at 10 nM concentration and from -60% to -28% at 0.5 nM concentration (p<0.01, Fig 3F). The gene discussed is VIP; the disease is infection.