KIT and acute myeloid leukemia: Sunitinib effectively inhibited the VEGF- or PDGF-mediated phosphorylation of VEGFR-2 and PDGFR-b, respectively, in NIH-3T3 cells (IC50 0.01 μM) [28], stem-cell factor (SCF)-induced phosphorylation of KIT in NCI-H526 human small cell lung cancer (SCLC) cells (IC50 0.001–0.01 μM) [29], FLT ligand-mediated phosphorylation of FLT3 expressed in RS4;11 and OSAML5 acute myeloid leukemia (AML) cells (IC50 0.25 μM) [30], and M-CSF-dependent phosphorylation in NIH-3T3 cells expressing CSF-1R (IC50 0.05–0.1 μM) [31].