Aberrantly high Bcl-2 expression is a common hallmark of DLBCL, predominantly affecting cases and genetic subtypes featuring (1) co-occurring MYD88/CD79 mutations and ABC-DLBCL origin, in which Bcl-2 overexpression is driven by gene amplification, or alternatively, featuring (2) BCL2 translocations, co-occurring activating EZH mutations and a GCB-DLBCL cellular origin. This evidence concerns the gene BCL2 and aneurysmal bone cyst.