Gilbert's syndrome (GS, MIM ID #143500) is defined as mild unconjugated hyperbilirubinemia, without liver disease or hemolysis, inherited in an autosomal recessive manner [Matsui et al. 2010]. Free bilirubin appears in the blood after breakdown of erythrocytes due to degradation of the heme ring and is eliminated by the liver after combination with glucuronic acid (direct conjugated bilirubin). This process is catalyzed by an enzyme: bilirubin-UDP-glucuronilotransferase UGT1A1, which is encoded by the UGT1A1 gene (MIM ID *191740, locus 2q37) [Strassburg 2010]. UGT1A1 participates in the second phase of xenobiotic inactivation mainly in the conjugation of bilirubin and marginally influences the activity of phenols, flavones, C18 steroids, food carcinogens, tobacco smoke and N-hydroxy-PhIP [Strassburg 2010]. Mutations in the UGT1A1 gene lead to Crigler-Najjar syndrome (type I and type II), and polymorphism of the 5-prime end of the UGT1A1 gene promoter is responsible for Gilbert syndrome. The homozygous wild type of the TATA box located in the promoter of the gene has six A(TA)6TAA repeats (UGT1A1*1/*1; 6/6), however in Gilbert syndrome seven are present in both A(TA)7TAA alleles (UGT1A1*28 /*28; 7/7), while the heterozygous variant has six UGT1A1*1/*28 repeats in one allele and seven in the second; 6/7 [Matsui et. to 2010]. It has recently been postulated that not only the TA insertion is responsible for GS but also other related polymorphisms such as c.-3275T>G (former name c-3279 T>G) present in the phenobarbital-responsive enhancer module [Mauro 2004; Matsui et. to 2010]. But the role of the mentioned polymorphism still remains unclear. The activity of the UGT1A1 enzyme in patients with GS is decreased to one third of normal activity, therefore an increased circulating concentration of serum bilirubin is evident...... half of the article ......the usefulness to modify an initial and/or subsequent dose of irinotecan in patients with metastatic CRC as a way to modify the rate of adverse drug events…”[Palomaki et al. 2009]. Dosage reduction of irinotecan could reduce ADRs, however it could lead to increased morbidity and mortality due to the “under-dosing” effect. Recently published data obtained from the Israeli population (329 colorectal cancer patients) showed a strong association between the 7/7 genotype of the UGT1A1 gene and severe toxicity and inferior overall survival in patients treated with irinotecan. Based on the available literature we can deduce that the study on the influence of the UGT1A1*28/*28 genotype are crucial for patients treated with irinotecan for predictions on their survival and survival. As far as we know, in Poland, in Lower Silesia, none Oncology center does not perform UGT1A1 test for patients.