Consistent with the model that GAB2 overexpression serves as an intermediate progression event between NPM1 mutations and downstream RTK/RAS signaling mutations, we observed that GAB2 expression was significantly higher in human AML with NPM1 mutations, and/or mutations in signaling genes, compared with other AMLs without these features, and/or healthy donor–derived CD34+ cells (Figure 8A). This evidence concerns the gene GAB2 and acute myeloid leukemia.