For example, while AML clones expressing FLT3(ITD) kinase seemed more responsive to the kinase inhibitor crizotinib, co-occurrence of DNMT3A mutation predicted resistance not only to the kinase inhibitor, but also to axitinib (P-glycoprotein efflux transporter inhibitor), cediranib (VEGFR inhibitor), ponatinib (ABL1 kinase inhibitor) and tofacitinib (JAK1/3 kinase inhibitor) [77]. This evidence concerns the gene DNMT3A and acute myeloid leukemia.