Thus, we focused on lenvatinib, which has a high affinity for RTKs, eg VEGFR2/KDR, VEGFR3/FLT4, VEGFR1/FLT1, PDGFRβ, FGFR1, PDGFRα or c‐Kit.22 Given that several target kinases such as PDGFRα and c‐Kit have been shown to play important roles in AML cell proliferation, we anticipated that lenvatinib should have a considerable anti‐AML effect. The gene discussed is FLT1; the disease is acute myeloid leukemia.