By conjugating lipophilic drugs to glucuronic acid (GlcA), UGTs impair biological activity and enhance water solubility of drugs, driving their elimination and a lack of drug efficacy.16 Accumulating evidence support an influence of the UGT pathway to drug resistance in many cancers including in leukaemias, namely in CLL patients treated with fludarabine and acute myeloid leukaemia (AML) patients receiving ribavirin or cytarabine-based treatments.17–19 However, for most drugs used in CLL, the glucuronidation pathway has not been comprehensively studied. The gene discussed is SLC35A2; the disease is B-cell chronic lymphocytic leukemia.