KMT2D and lymphoma: Although GCB-DLBCL and FL represent two clinically and histopathological distinct lymphoma entities, it has become apparent that these two subtypes are far more intricated from a genetic point of view as illustrated by shared multiple recurrent genetic lesions such as BCL2 alterations, mutations in epigenetic regulators (KMT2D, CREBBP, EZH2, EP300...) and immune receptor signaling genes suggesting at least clonal evolution from a similar precursor cell and shared oncogenic pathways (53, 56).