CPT-11 is activated by hydrolysis to SN-38 that is primarily inactivated through biotrans-formation into SN-38 glucuronide ( SN-38 G) by UGT1As. Tailoring chemotherapy based on the genetic profile of patients and tumor would increase efficacy and decrease toxicity for patients. The toxicities of CPT-11 have been reported to correlate with the polymorphism of the number of TA repeats in UGT1A1 gene because of its gene transcriptional efficiency. UGT1A1*28 was chosen as the candidate gene to be investigated as a predictor of severe toxicity. Other studies determining predictive markers of CPT-11 efficacy have been highly controversial.