BCL6 and lymphoma: In contrast, definitive silencing of BCL6 is mediated by GC exit regulators such as IRF4 and later PRMD1, as well as through BCL6 protein degradation by FBXO11, to enable full resolution of the GC phenotype and terminal differentiation.90, 91 These mechanistic considerations help to explain the various ways in which BCL6 functions are reinforced and maintained by lymphoma somatic mutations.