This observation is consistent with the hypothesis that AML cells survive in CXCL12‐rich BM niches,2 while chemoresistant T‐ALL cells localize stochastically.5 To understand the importance of the CXCL‐12/CXCR4 axis, we monitored the short‐term effect of CXCR4 inhibition by performing timelapse intravital microscopy of the same BM areas before and after administering AMD3100 (plerixafor, 4 mg kg−1, I.V.; Figure 2d). This evidence concerns the gene CXCR4 and acute lymphoblastic leukemia.