Whole-genome sequencing revealed that each tumor acquired 1 or more human AML-like cooperating mutations, including RTK/RAS signaling mutations in Ptpn11 (E69K, A72V, A465T, or S506L), Kit (D818Y), Cbl (Y369H, Q365K, or exon 9 deletion), Nf1 (frameshift), and a focal (2.5 Mbp) amplification of chromosome 5 that included Flt3, associated with more than 20-fold overexpression of that gene (Figure 1A and Supplemental Table 1; supplemental material available online with this article; https://doi.org/10.1172/JCI195929DS1). The gene discussed is PTPN11; the disease is neoplasm.