In accordance with this observation and the TOX mutations in ABC-DLBCL, GEP analyses revealed high TOX expression associated with GCB-DLBCL signatures and proliferation cascades, while low expression correlated with post-GC B-cell signatures, and myeloma and plasma cell programs, also potentially suggesting a relevant role for TOX as a negative regulator of the late B-cell differentiation program. The gene discussed is TOX; the disease is aneurysmal bone cyst.