Our data suggest that CCL5 release is one factor that contributes to FLT3‐TKI resistance, possibly via Stat5 or PI3K/Akt and Bcl‐2 signaling in vitro and is upregulated ex vivo in blasts from FLT3 mutated AML patients preceding failure to FLT3‐TKI therapy. This evidence concerns the gene CCL5 and acute myeloid leukemia.