Notably, TET2 and CREBBP mutations are mutually exclusive in DLBCL.45 EZH2 mediates the transient repression of gene promoters in a BCL6‐dependent manner.47 EZH2 mutation results in enzymatic gain of function, and in vivo EZH2 mutant models show GC hyperplasia and lymphomagenesis.48 The gene discussed is BCL6; the disease is diffuse large B-cell lymphoma.