Overexpression of Gab2 leads to increased metastatic potential with anchorage independence in soft agar, and a previous report revealed that the cooperative activity of Gab2 in NRAS-driven melanoma increases anchorage independent growth by improving survival of Gab2-expressing cells, enhancing tumorigenesis in vivo and facilitating an angiogenic switch through the upregulation of HIF-1a and VEGF by MAPK signaling, but not PI3K signaling, in Gab2/NRAS-driven tumorigenesis (47). This evidence concerns the gene NRAS and melanoma.