Given that TNF is a well-known glycolytic inducer, we propose that in combination with TNF-induced MAS inactivity, TNF-activated glycolysis will be further accelerated by (1) enhanced LDHA activity responsible for NAD+ regeneration, and (2) by diminished mitochondrial pyruvate-driven respiration due to restricted mitochondrial NADH availability, all leading to excessive lactate production in TNF-induced SIRS. Here, TNF is linked to systemic inflammatory response syndrome.