With the activation of the Flt3 signaling pathway in the presence of activating factors, this IL-3 independent growth advantage was enhanced, suggesting that the loss of N-CoR mediated Flt3 repression in AML-M5 may have resulted in the aberrant expression of Flt3 and could enhance the survival and proliferation of AML-M5 blasts in the presence of factors or mutations which activate the Flt3 signaling pathway. The gene discussed is FLT3; the disease is acute myeloid leukemia.