CLL B-cells express VEGF receptors and respond to VEGF stimuli by upregulating the myeloid cell leukemia 1 gene (MCL1) and the X-linked inhibitor of apoptosis protein XIAP. Thus, miR-92-1 overexpression enhances the VEGF autocrine pathway for cell survivorship, suggesting that VEGF inhibition may be a promising new therapeutic approach in CLL [51,52]. Here, VEGFA is linked to B-cell chronic lymphocytic leukemia.