Furthermore, FGF2-FGFR1 signalling has been shown to be selectively activated in the bone marrows of patients with AML, favoring the survival of leukemia cells, progression, and therapy resistance, and that FGFR inhibition could reserve the stromal protection of leukemia cells and overcome resistance to kinase inhibitors [21]. This evidence concerns the gene FGFR1 and acute myeloid leukemia.