In clinical samples it was shown that activating mutations in FLT3 (FLT3 amplifications occur in about 30% of AML patients) were associated with high β-catenin levels [30] and that expression of total β-catenin, and more specifically non-phosphorylated nuclear β-catenin, correlated with a poor overall survival in AML patients [18,31]. This evidence concerns the gene FLT3 and acute myeloid leukemia.