The dependence of ABC-DLBCL from the BCR signaling pathway is underscored by the preferential sensitivity of these tumours to pharmacological agents that inhibit Bruton tyrosine kinase (BTK), the molecule linking the BCR to the NF-κB pathway, even in the absence of mutations targeting the BCR subunits CD79A/B [97]. This evidence concerns the gene NFKB1 and diffuse large B-cell lymphoma.