The analysis of sub-clusters (dependent on driver mutations) of DLBCL samples suggested that those driven by direct activators of NF-κB signaling (e.g. an ‘MyD88-like’ sub-cluster, see Methods) had a lower ratio of alternative splicing vs canonical, and specifically isoform 3, than those driven by indirect NF-κB activation (e.g. BCL2-, BCL6- and TP53-like DLBCL, see Figures 2F and S2E). This evidence concerns the gene BCL2 and diffuse large B-cell lymphoma.