Although the mechanism of Treg recruitment in AML has not been thoroughly investigated in humans, AML patients show much higher expression of CXCR4 (the receptor for CXCL12) in Treg compared to healthy individuals [57], suggesting that the CXCL12–CXCR4 axis may be more significant for Treg recruitment in AML patients than CCL3. The gene discussed is CXCR4; the disease is acute myeloid leukemia.