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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Eur J Med Chem. 2015 Feb 28;94:123–131. doi: 10.1016/j.ejmech.2015.02.052

Fig. 1.

Fig. 1

In AML, the FLT3 receptor tyrosine kinase becomes constitutively active and stimulates RAS/RAF, JAK/STAT, and PI3K/AKT pathways. This modifies the apoptotic signaling axis, which causes cell survival and proliferation.