As recently reviewed [56], the literature on the importance of miRNAs deregulation in creation of mouse models of lymphocytic leukemias is becoming increasingly richer. Early this year, Dalla-Favera and colleagues published the genetic validation that deletion of miR-15a/16-1 leads to CLL in mice [57]. In order to identify the genetic elements targeted by the putative 13q14 tumor suppressor and to determine their contribution to the pathogenesis of CLL, they generated knockout mice that carried conditional alleles that either mimicked the deletion of the minimal deleted region (MDR), previously described in human CLL [9, 58] and comprising the entire Dleu2 gene, or that specifically deleted the miR-15a/16-1 cluster without affecting the expression of Dleu2. At the age of 2–4 months, homozygous Mdr−/− and miR-15a/16-1−/− mice showed normal percentages of B and T cell subpopulations and normal development of lymphoid organs. However, one year old Mdr−/− mice showed higher percentages of CD5+B220 B cells among mononuclear cells in the peritoneal cavity (50% vs. 15% in controls). Similar observations were made in miR-15a/16-1−/− rodents. Thus, deletions of the Mdr and miR-15a/16-1 are associated
