AML cells hijack the BM niche by upregulating receptors on their cell surface, such as very late antigen-4 (VLA-4), CD44, E-selectin ligand-1 (ESL-1), and CD98, resulting in the retention of LSCs in the BM niche via interactions with adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), fibronectin (FN), hyaluronan (HA), osteopontin (OPN), selectins, and integrins. Here, GLG1 is linked to acute myeloid leukemia.