Our observations in CLL patients treated with fludarabine raised the possibility that UGT2B17 may be involved in the glucuronidation of the drug itself, and potentially also of B-cell receptor inhibitors ibrutinib and idelalisib, which contain functional hydroxyl and amino groups susceptible for conjugation into inactive glucuronides (G). Here, UGT2B17 is linked to B-cell chronic lymphocytic leukemia.