In view of the role of SETD2 disruption in tumorigenesis and the identification of SETD2 abnormalities in our discovery cohort, we then accrued samples from other patient cohorts, including the GCLLSG CLL8 cohort in which 3p deletions had also been detected,18 to confirm the incidence of SETD2 disruption and evaluate its biological and clinical consequences in CLL. This evidence concerns the gene SETD2 and B-cell chronic lymphocytic leukemia.