Its mechanism of action involves the inhibition of the tyrosine kinase activity of VEGF, platelet-derived growth factor receptor-β, KIT (stem cell factor receptor), FMS-like tyrosine kinase-3 receptor (FLT-3) and rearranged during transfection (RET); it consequently specifically blocks signal transduction associated with these kinases to exert anti-tumor effects. This evidence concerns the gene VEGFA and neoplasm.