In DLBCL, some gain-of-function mutations generate chronic activators of NF-κB (e.g., mutations in CD79, MYD88, or REL gene amplification), whereas other loss-of-function mutations inactivate negative regulators of NF-κB (e.g., IκB, CYLD, A20, TRAF3) [19,20]. The gene discussed is MYD88; the disease is diffuse large B-cell lymphoma.