Similar to other oncogenes, including BRAFV600E or KRASG12D in solid tumors8,9,28,29 or BCR-ABL in chronic myelocytic leukemia11 and FLT3-ITD in AML16, our study shows that activating mutations of the tyrosine-kinase receptor KIT triggers autophagy and supports cell proliferation and survival in AML cells. This evidence concerns the gene KIT and acute myeloid leukemia.