These findings broaden the scope of CREBBP-mediated enhancer regulation beyond current knowledge based on its ability to acetylate H3K18 and H3K27, and have implications for the understanding and therapeutic targeting of the early phases of FL/DLBCL pathogenesis, where mutations inactivating these enzymes are coselected at high frequency. This evidence concerns the gene CREBBP and diffuse large B-cell lymphoma.