CYP2E1 and tuberculosis: Prolonged clinical treatment with INH is the most common cause of liver injury in patients receiving anti-TB therapy [4]. In the liver, N-acetyltransferase 2 enzyme metabolizes INH to acetyl INH, which subsequently hydrolyses into acetyl-hydrazine (AcHz), which is further oxidized by cytochrome P450 2E1 (CYP2E1) to form highly reactive acetylating hepatotoxic intermediates, causing hepatocellular degeneration [5].