NCOR1 and acute myeloid leukemia: These findings, along with our previous report demonstrating a key role of Akt in N-CoR misfolding (9), suggest that Akt activation may act as a bridge between the extracellular oncogenic stimulus and N-CoR-based transcriptional machinery to dynamically regulate the expression of self-renewal genes during normal hematopoiesis and AML pathogenesis.