The latter mechanism appears to be particularly frequent in MZL and ABC DLBCL, where the NF-κB pathway is activated either by BTK-distal events, such as genetic lesions in BCL10, MALT1, and CARD11, or by genetic lesions in the non-canonical pathway, such as mutations in BIRC3 and TRAF3. The gene discussed is BTK; the disease is diffuse large B-cell lymphoma.