Compared with the paired CLL, RT samples were characterized by increased mutational burden mainly related to some genes previously unrecorded in CLL (BDKRB1, WWP1, TFCP2, SVIL, SLC9B1, RELN, PTK2, IRF2BP2, IL7) (45), and whose role in RT pathogenesis needs to be clarified by functional studies. The gene discussed is PTK2; the disease is B-cell chronic lymphocytic leukemia.