They combined BCL2/MYC and NFKBIA, a surrogate marker of NFKB activity [55], and confirmed the clinical applicability of GEP techniques to DLBCL patient stratification and the value of combining markers measuring BCL2/MYC expression with others recognizing the contribution of COO (our model) or NF‐kB activity (Derenzini's model) [55]. The gene discussed is MYC; the disease is diffuse large B-cell lymphoma.