This phenomenon was first demonstrated in ABC‐DLBCL using a loss‐of‐function RNA interference screen to identify dependence on BCR signaling mediators.136 Following this effort, a number of reports confirmed the presence of somatic mutations in BCR pathway genes such as TNFAIP3, CARD11, and CD79A/B (Figure 4).137, 138, 139 For example, FL and ABC‐DLBCL (C5 and MCD cases) preferentially carry mutations in genes characteristic of active BCR signaling (eg, CD79A/B or CARD11). The gene discussed is TNFAIP3; the disease is diffuse large B-cell lymphoma.