It is possible that the SETD2 alterations present in our CLL cases may contribute to further inactivation of p53-mediated checkpoint control, a situation that has been proposed in clear cell renal cell carcinoma.8 The low frequency of SETD2 disruption and the association with TP53 abnormalities hinder an accurate assessment of its clinical consequences. The gene discussed is TP53; the disease is B-cell chronic lymphocytic leukemia.