The primary biological functions of SLC25A21 were suppressed after CXCL8 overexpression in vitro, confirming the tumor-promoting action of CXCL8. The exact mechanism by which the SLC25A21 regulates CXCL8 in AML remains unclear, and much work needs to be done in our subsequent studies. The gene discussed is CXCL8; the disease is acute myeloid leukemia.