Variations (polymorphisms) in the N-acetyltransferase 2 (NAT2) gene, responsible for the metabolism of isoniazid was significantly associated with the likelihood of experiencing TB drug related hepatotoxicity.22 A randomised controlled trial demonstrated that the risk of drug-induced liver injury due to isoniazid could be reduced in adult slow acetylators by a dose reduction to 2.5 mg/kg/day without early treatment failure.23 This evidence concerns the gene NAT2 and tuberculosis.