Another analysis of the same property associated with marmesin (33), but on lung cancer and tumor angiogenesis, reports anti-tumor activities of marmesin (33) mediated by the inactivation of mitogenic signaling pathways and negative regulation of proteins related to cell signaling, including vascular endothelial growth factor-2 receptor (VEGFR-2), integrin β1, integrin-linked kinase (ILK) and matrix metalloproteinases-2 (MMP-2), nullifying mitogen-stimulated proliferation and invasion in cells expressing p53 or not [112]. Here, TP53 is linked to neoplasm.