ABC-DLBCL is mainly dependent on BCR signalling for survival and proliferation: approximately 10% of cases demonstrate mutations in CARD11, resulting in constitutive downstream activation of NF-kB; 20% of cases harbour mutations in the ITAM of CD79A and CD79B, resulting in downstream kinase activation of SYK, BTK, PI3K, and PKCβ; and 30% of cases have MYD88 L265P mutations that directly activate the NF-κB pathway. This evidence concerns the gene CD79B and aneurysmal bone cyst.