In the absence of oncogenic Ras mutations, alternative mechanisms activating Ras, such as oncogenic activation of upstream tyrosine kinases as seen in AML cells [56], [57], [58], [59] and loss-of-function mutations in the Ras-GAP protein; neurofibromatosis 1 as seen in juvenile myelomonocytic leukemia (JMML) [60], have been suggested. This evidence concerns the gene NF1 and acute myeloid leukemia.