Yu et al84 introduced a novel AML xenograft model in zebrafish and indicated that loss of function of CD44, which physically associates with CXCR4 at the cell membrane upon CXCL12 induction, sensitizes AML cells to the venetoclax through abrogating CXCL12‐mediated survival signaling. This evidence concerns the gene CXCR4 and acute myeloid leukemia.