These results demonstrate that, in addition of the previously known antiangiogenic effect of sunitinib produced by direct inhibition of VEGFR in endothelial cells, this drug has an indirect inhibitory effect of PI3K/Akt pathway that results in an increase of MYCN protein the degradation and the consequently decrease in VEGF secretion by MYCN amplified tumor cells. This evidence concerns the gene MYCN and neoplasm.