This was also shown in the 3D BM vascular model developed by Bray et al., where both AML cell lines (KG1a, MOLM13, MV4-11, OCI-AML3) and primary patient-derived AML cells exerted preference to adhere and proliferate along the endothelial network (HUVECs-BM-SCs), further highlighting the importance of the interaction between AML cells and the vascular niche. This evidence concerns the gene RUNX2 and acute myeloid leukemia.