The cases expressing DLBCL signatures had a significantly higher genomic complexity (estimated as % aberrant genome) compared with cases with mBL, but comparable with de novo DLBCL (Figure 2A), suggesting more genetic alterations are essential for lymphomagenesis or aggressive clinical behavior as observed in DLBCL, but unlike BL which predominantly driven by t(8;14) or constitutive MYC oncogene overexpression. This evidence concerns the gene MYC and diffuse large B-cell lymphoma.