In the case of our two patients, the reactivation of EBV paralleled evolution of LDH as a marker of aggressive transformation of CLL (Figures 1 and 2). Treatment with rituximab alone to target EBV replication in B-lymphocytes, as inspired by treatment regimens for post-transplant lymphoproliferative disorders (PTLD), resulted in a clear regression or even CMR in both patients [[14]]. EBV and Richter syndrome (RS) represent a well-known association although it is not entirely clear whether EBV infection is a causal element leading to RS and/or a consequence of the immunosuppressive state associated with CLL and its treatment [[1]]. [Extracted from the article]