As previously described, upregulation of AXL has been implicated as a mechanism of resistance to FLT3 inhibition in AML and a dual FLT3/AXL inhibitor (ASP2215) is currently in clinical development, making further evaluation of MRX-2843 as a dual MERTK/FLT3 inhibitor particularly attractive. This evidence concerns the gene FLT3 and acute myeloid leukemia.