The genomic landscape of non-GCB DLBCL has been well characterized, with oncogenic driver mutations typically affecting NF-kB and B-cell receptor (BCR) activation.5,6 Conversely, GCB DLBCL often involves constitutive activation of BCL2, preventing apoptosis.5 The differences between the 2 groups have important prognostic implications, as non-GCB DLBCL is a predictor of poor response to R-CHOP.7 Previous studies have demonstrated that most PCL cases are of the non-GCB subtype.8 This evidence concerns the gene NFKB1 and diffuse large B-cell lymphoma.