As DLBCL can be driven by BCL6 translocations or hyperactive RAS signaling [54], the appearance of frequent mutations in Kras or Bcor, which encodes a repressor of BCL-6, as tertiary drivers in Eμ-Myc lymphomas might explain DLBCL-like gene expression signatures [24]. This evidence concerns the gene BCOR and diffuse large B-cell lymphoma.