More specifically, CLL cell-derived EVs activated the AKT/mammalian target of rapamycin/p70S6K/hypoxia-inducible factor-1 alpha axis in CLL-BMSC, which resulted in excessive production of the vascular endothelial growth factor, a survival factor for CLL-B cells [55]. The gene discussed is HIF1A; the disease is B-cell chronic lymphocytic leukemia.