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. The gene discussed is FLT3; the disease is acute myeloid leukemia.