In AML cells, the FLT3-ITD fusion protein with tyrosine kinase activity encoded by the mutation of the FLT3-ITD gene activates the downstream STAT5-PIM, PI3K-AKT and other cell signaling channels, resulting in accelerated proliferation of leukemia cells, thereby inducing DNA replication stress1. Here, FLT3 is linked to acute myeloid leukemia.