Remarkably, high-dose thiamine therapy prevented hepatic steatosis induced by overnutrition in sheep [18], and restored reduced mitochondrial TPP-dependent enzymatic activities associated with traumatic brain injury even in the absence of thiamine deficiency [35], together suggesting that thiamine concentrations higher than the normal physiological levels may boost mitochondrial combustion, presumably though not necessarily exclusively by maximizing the oxidative capacity of TPP-dependent mitochondrial dehydrogenases. This evidence concerns the gene TNS3 and brain injury.