VLA-4, upon interaction with VCAM-1, activates pro-survival and proliferative pathways in both AML and stromal cells via the nuclear factor kappa B (NF-κB) pathway, leading to chemotherapy resistance due to protection from apoptosis [42,43] as it allows for complete integration into the vascular niche and confers a quiescent phenotype to AML cells [44]. Here, VCAM1 is linked to acute myeloid leukemia.