Somatic alterations involving genes of tumor suppression, cell cycle and proliferation pathways (i.e., mutations or disruptions of TP53, NOTCH1, MYC, and CDKN2A) are the main genetic clues of DLBCL-RT and can explain its aggressive disease kinetics and chemoresistance (30, 37, 38). This evidence concerns the gene TP53 and diffuse large B-cell lymphoma.