We have previously shown that N-CoR is a direct target of heterogeneous oncogenic insults such as fusion oncogenes created by chromosomal translocations, which trigger a nearly homogenous change in N-CoR conformation through aberrant post-translational modification, ultimately leading to its misfolding and premature loss in promyelocytic and monocytic AML, two distinct subtypes of AML characterized by maturation arrest of intermediate myeloid cells (4–9). The gene discussed is NCOR1; the disease is acute myeloid leukemia.