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. This evidence concerns the gene SVIL and B-cell chronic lymphocytic leukemia.