The CXCR4 expression percentage with FLT3‐ITD mutant was significantly higher than the group with wild type, consistent with previous research.18 This suggests that FLT3‐ITD mutation and CXCR4 may have possible interaction, such as FLT3‐ITD mutation can activate CXCR4 shift signal, and stromal cells cocultured with FLT3‐ITD leukemia cell can weaken FLT3‐ITD mutation inhibitors for cell apoptosis. The gene discussed is CXCR4; the disease is leukemia.