We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal-promoting effects in human cord blood CD34(+) cells and its leukemogenicity in mouse models.     ///    The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation..     ///    Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. 