On the contrary, AML cells upregulate CXCR4, VLA-4, CD44, E-selectin, and CD98 adhesion molecules [45,52], and LSC rely on CXCL12/CXCR4 and integrin/OPN signaling for their adhesion and persistence, on Wnt/β-catenin and PI3K/Akt signalings for their self-renewal and maintenance [63], and on SIRPα/CD47 binding for their survival and functionality [64]. The gene discussed is CXCR4; the disease is acute myeloid leukemia.