In vitro experiments support the oncogenic role of miR-125b, as it seems to repress BCL2 (and thus promote proliferation in response to CD40 ligand, i.e., CD154 in human leukemic B-cells) and to enhance proliferation and block differentiation by targeting ARID3A (AT-rich interaction domain 3A or BRIGHT, i.e., B-cell regulator of immunoglobulin heavy-chain transcription) in t(11;14)(q24;q32) B-ALL [109,110]. This evidence concerns the gene ARID3A and precursor B-cell acute lymphoblastic leukemia.