More specifically, a gain-of-function mutant of EZH2 (Y641F), which is also found among B-cell lymphoma patients [54,87], acted in concert with wild-type EZH2 to elevate activating H3K27 trimethylation marks in Eμ-Myc transgenic mice, resulting in enforced B-cell receptor signaling and lethality [86]. This evidence concerns the gene MYC and B-cell non-Hodgkin lymphoma.