In most ABC-DLBCL cases, the activity of the canonical NF-κB transcription complex is sustained by the presence of genetic alterations affecting multiple genes that encode for positive or negative regulators of the BCR, CD40 receptor, and TLR signaling cascades, with the TLR adaptor protein MYD88 being mutated in over 30% of patient samples (157–160). This evidence concerns the gene MYD88 and aneurysmal bone cyst.