With this aim we took advantage of primary and derived compound mutant murine lymphomas from the Eμ-myc transgenic mouse model of B-cell lymphoma18, 24, 25 and human B-cell lymphoma lines with matched isogenic chemotherapy/rituximab resistant cell lines.26 To delineate the pathways required by BETI, we used I-BET762 compound, a potent inhibitor of BET bromodomain proteins,13 and evaluated its ability to mediate apoptosis in the different models. This evidence concerns the gene MYC and B-cell non-Hodgkin lymphoma.