Further in vitro and in vivo studies demonstrated that SFN inhibits cell surface tyrosine kinase receptors (e.g. VEGFR-1, VEGFR-2, VEGFR-3; PDGFR-b, c-KIT, FLT-3 and RET) and downstream intracellular serine/threonine kinases of the RAF/MEK/ERK pathway (e.g. Raf-1, wild-type B-Raf, and mutant B-Raf) leading to a dual mechanism of action by targeting tumor cell proliferation and tumor angiogenesis (Wilhelm et al., 2004; Wilhelm et al., 2006; Gadaleta-Caldarola et al., 2015). This evidence concerns the gene SFN and neoplasm.