These findings suggest that transcriptional repression mediated by N-CoR might be crucial for the suppression of self-renewal potentials of primitive hematopoietic cells during their commitment and maturation to cells of myeloid lineage, and abrogation of this repression due to the misfolding and premature loss of N-CoR may contribute to the formation of LSC or LIC through the ectopic reactivation of CD34+/Flt3+-based stem cell phenotype in promyelocytic and monocytic AML. The gene discussed is NCOR1; the disease is acute myeloid leukemia.