BCL2L11 and graft versus host disease: EZH2 has been found to be enriched in chromatin damage sites, and EZH2 deficiency accelerates effector Th-cell death via death receptor-mediated extrinsic and intrinsic apoptotic pathways.8 Our previous study has also demonstrated that inhibition of EZH2 arrests ongoing graft-versus-host disease by inducing apoptosis in alloreactive T cells and that this induction of apoptosis is largely independent of the proapoptotic protein Bim.9 Interestingly, the underlying mechanism remains unclear.