A variety of mechanisms are involved in this aberrant activity, including mutations in CARD11, found in approximately 10% of ABC-DLBCL; loss of function mutations in A20 (a NF-κB negative regulator), found in about 24% of ABC-DLBCL; and ITAM mutations, present in approximately 20% of ABC-DLBCL, which prevent BCR endocytosis and cause an increase in BCR expression and a decrease in LYN kinase activity [40,41,42]. The gene discussed is BCR; the disease is aneurysmal bone cyst.