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 SLC9B1 and B-cell chronic lymphocytic leukemia.