The mechanisms involved in activation of this pathway have been examined in AML and ALL and include activating mutations of the FLT3 and the KIT tyrosine kinase receptors, NRAS or KRAS mutations, PI3K overexpression [40], low levels of PP2A phosphatase activity and autocrine/paracrine secretion of growth factors such as IGF-1 and VEGF [23]. This evidence concerns the gene IGF1 and acute myeloid leukemia.