 The histidine to tyrosine mutation at residue 268 is located in the N-terminal portion of UGT2B7, which binds the xenobiotic substrate as opposed to the C-terminus which binds UDP-glucuronic acid.The speculated mechanism for this increased cancer risk involved increased glucuronidation of benzidine by the mutant UGT2B7 followed by cleavage of the glucuronidated benzidine at urine pH levels, releasing higher concentrations of benzidine in the bladder.Another study looked for a similar association of variant UGT2B7 G900A with the risk of colorectal cancer but found no significant association.