CircMYBL2 knockdown specifically suppressed FLT3‐ITD AML proliferation and promoted its differentiation, and also damaged cytoactivity of inhibitor‐resistant FLT3‐ITD‐positive AML,7 suggesting circMYBL2 as a possible target for FLT3‐ITD AML treatment.28 This evidence concerns the gene FLT3 and acute myeloid leukemia.