As in AML patients, redundant activation of multiple signal transduction pathways, such as PI3K/AKT, MAPK, and JAK/STAT, was observed and linked to poor prognosis early on, the targeting of the oncogenic signal at more than one level in FLT3-targeted therapies has been long recognized as a promising strategy for AML treatment [64]. The gene discussed is FLT3; the disease is acute myeloid leukemia.