In most cells, β-catenin is constantly degraded in the cytoplasm, but β-catenin stabilization upon WNT signaling promotes its function as co-activator of TCF/LEF transcription in the nucleus.16 Deregulations in WNT signaling and enhanced β-catenin amounts are found in many human cancers including hematologic malignancies.17, 18 We show here that stabilization of β-catenin by oncogenic CARMA1 engages a novel cross-talk between NF-κB and WNT pathways in DLBCL that can contribute to ABC DLBCL lymphomagenesis. The gene discussed is CARD11; the disease is aneurysmal bone cyst.