VEGFB and neoplasm: Interestingly, we have found that this tumor growth/dissemination antagonism, as regulated by RAS sublocalization, is orchestrated by a VEGF-B autocrine loop in such a way that high VEGF-B levels promote big tumors with reduced propensity for dissemination, whereas curtailing VEGF-B secretion results in smaller tumors, though with enhanced metastatic potential.