VAV1 and neoplasm: We demonstrated here the ability of the Vav1-induced miR-29b to down-regulate Akt2 in MDA-MB-231 cells both in vitro and in tumor xenografts derived from MDA-MB-231 cells stably over-expressing Vav1, ascertaining the existence of a Vav1/miR-29b/Akt2 axis in these TNBC cells.