As shown for RAS, coexpression of Ptpn11S506W and Ptpn11E67k accelerated KMT2A-MLLT3 leukemia development in syngenic mouse models.74,78 In vitro studies have demonstrated that SH2 and PTB domains PTPN11 mutants such as PTPN11E76K, PTPN11A72V, PTPN11D61Y, and PTPN11G503A lose the autoinhibitory feedback, increased phosphatase activity, and induced hypersensitivity to IL-3 and GM-CSF. This evidence concerns the gene KMT2A and leukemia.