Approximately 20% of acute myeloid leukemia (AML) patients have been found to have constitutive activation of the FLT3-receptor tyrosine kinase due to internal tandem duplications of the juxtamembrane domain (FLT3-ITD). Yamamoto and colleagues (page [2434][1]) now report that Asp835 in the kinase
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James D. Griffin (2001) studied this question.