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. The gene discussed is TNS3; the disease is Thiamine deficiency.