MYB and acute myeloid leukemia: Such inhibition relies on interaction between a common PXLXP motif present in E1A, EBNA2 or MYB and ZMYND11’s MYND domain, a C-terminal module lost in the AML-associated ZM chimera; in addition, ZMYND11’s MYND domain recruits additional repressors such as Nuclear Receptor Corepressor (N-CoR) and histone deacetylase (HDAC) complexes16,17.