The rates of discontinuation due to AEs were 5.0% in the ASCENT study in metastatic breast cancer, and 11.0% in the SASCIA study in early breast cancer.82,90 The genetic polymorphism UGT1*28/28 is involved in the metabolism of SN38 and is associated with a higher risk of AEs, particularly neutropenia.93 UGT1A1 genotyping or a primary prophylactic use of granulocyte colony-stimulating factor could be considered in some cases. This evidence concerns the gene UGT1A1 and breast carcinoma.