Other studies have suggested the involvement of genetic risk factors for hepatotoxicity when anti-TB drugs are used: namely, the slow acetylator phenotype of the Arylamine N-Acetyltransferase (NAT2) gene, the heterozygous c1/c2 and the homozygous c1/c1 for cytochrome (CYP) 2E1, the absence of human leukocyte antigen (HLA)-DQA1*0102 and the presence of HLA-DQB1*0201 [12–14]. This evidence concerns the gene NAT2 and tuberculosis.