Apart from the HLA alleles, drug-metabolizing enzymes may be a risk factor for developing CADR. LTG is primarily metabolized by uridine diphosphate glucuronosyltransferases (UGT), including UGT1A4 and UGT2B7 (Perucca, 2006). 2-N-Glucuronide conjugates are the major inactive metabolite of LTG and elimination from the body by any enzyme variant either than one of these UGT enzymes will affect the risk of cutaneous adverse drug reactions (Rowland et al., 2006). A recent study on drug metabolizing enzymes found that the cytochrome P4502C9 (CYP2C9) influenced PHT-induced SCAR in the Thai population (Tassaneeyakul et al., 2016). Further association studies are required to determine the association between the glucuronidation metabolic pathway and LTG-induced CADR.