Furthermore, the persistence or even up-regulation of PI3K/AKT/mTOR and MAPK/ERK pathways were shown in both FLT3 inhibitors-resistant FLT3-ITD AML cell lines and primary AML blasts despite inhibition of FLT3 phosphorylation by FLT3 inhibitors, suggesting that at resistance, some AML cells become independent of FLT3 signalling [47,48]. Here, FLT3 is linked to acute myeloid leukemia.