To identify genes that, when cotargeted, produce a phenotypic effect that can enhance the effect of midostaurin treatment in AML patients, we conducted genome-wide loss-of-function screens with the human CRISPR knockout (KO) pooled library “Brunello” from the Broad Institute (Addgene#73179) [12] applying selective pressure with midostaurin, a multikinase inhibitor with high specificity for mutant FLT3, but not wildtype FLT3. This evidence concerns the gene FLT3 and acute myeloid leukemia.