Recently, the molecular mechanism which mediates N-CoR loss in AML-M5 have been elucidated in our laboratory (Nin et al, submitted manuscript) and we have also identified several small molecules which were able to target this mechanism to restore N-CoR function and inhibit cellular growth in AML-M5, suggesting that N-CoR could pose as a plausible candidate for therapeutic targeting in AML-M5 independent of the Flt3 receptor status. The gene discussed is NCOR1; the disease is acute myeloid leukemia.