Since UGT1A1 plays a central role in the chemical modification of both bilirubin and the active metabolite of irinotecan, it has been suggested that pretreatment serum bilirubin levels in cancer patients reflect underlying UGT1A1 polymorphisms and thus serum bilirubin may substitute for UGT1A1 genotyping to risk-stratify patients for the occurrence of irinotecan-related toxicity (e.g., severe neutropenia) [21]. The gene discussed is UGT1A1; the disease is Decreased total neutrophil count.