Excitingly, from a therapeutic standpoint, our data demonstrate that, while genetic disruption of Prdm15 has similar effects to the inhibition of Igf1R/InsR (linsitinib) and mTORC1 (everolimus), PRDM15 null cells fail to activate alternative proliferative pathways, leading to a more efficient and durable killing of B-cell lymphomas. This evidence concerns the gene IGF1R and B-cell non-Hodgkin lymphoma.