PTPN11 (SHP2) gain-of-function mutations block autoregulation of SHP2 catalytic activity, leading to uncontrolled hyperactivation of the RAS/RAF/MAPK and JAK/STAT5 pathways, resistance and poor overall survival, which have also been identified in myeloid leukemia [46, 47]. This evidence concerns the gene RAF1 and myeloid leukemia.