HGS and neoplasm: Similarly, increased miR-296 expression activates angiogenesis in cultured ECs due to the suppression of HGS (hepatocyte growth factor-regulated tyrosine kinase substrate) which mediates VEGFR-2 and PDGFR-β (platelet derived growth factor receptor beta) degradation, whereas miR-296 inhibition reduces angiogenesis in tumour xenografts [120].