In the 26% of leukemia cases that do show clonal evolution, there may be somatic drivers involved, such as NOTCH1 or chr11 deletions (including the interval encoding ATM), as has been suggested by previous work.36 We observed three instances of 11q deletions occurring in leukemias that showed clonal evolution, with two instances arising during progression, findings consistent with a late-acting role for ATM. Both ATM and TP53 are DNA damage response genes recurrently mutated or deleted in CLL and associated with poor prognosis. Here, ATM is linked to B-cell chronic lymphocytic leukemia.