Using a retroviral infection system of shRNAs transduction to silence Kmt2d in HSPCs from VavP-Bcl2 donor mice following transplantation into irradiated wild-type mice, an acceleration of the lymphomagenesis process as well as an increase in the incidence of FL-like tumors (from 30 to 60%) was observed in double-mutant mice compared to shRNA control vectors, validating the tumor suppressive role of Kmt2d in B lymphocytes. Here, BCL2 is linked to neoplasm.