In this framework, constitutive activation of the NF-κB signaling pathway downstream of a chronic active (e.g., antigen-dependent) BCR represents a genetic and phenotypic hallmark of ABC-DLBCL (MCD and/or BN2), where both the canonical [Figure 3] and non-canonical pathway are hijacked by a variety of genetic alterations (see next section). The gene discussed is NFKB1; the disease is diffuse large B-cell lymphoma.