In injured brain cells, PDH is believed to be inactive and therefore contributes to the hyperglycemia and lactic acidosis due to reduced glucose metabolism.[6, 7] Pyruvate has been widely recognized as a metabolic substrate with multiple antioxidant properties and a natural allosteric stimulator of PDH, but its effects on TBI are not known.[8–11]. The gene discussed is PDP1; the disease is lactic acidosis.