To address the questions outlined above, we used intravital microscopy of calvarium BM to study the biology of AML in the BM using the well‐established preclinical model of MLL‐AF9‐driven AML.14 We characterized (1) migration of AML cells in vivo prior to and following chemotherapy, (2) expression of CXCR4 of early infiltrating and chemoresistant cells, and (3) the role of CXCR4 inhibition on the biology of AML within the BM. The gene discussed is KMT2A; the disease is acute myeloid leukemia.