For instance, ADM induces EC proliferation and tumor angiogenesis and growth [131], PGE2 enhances EC motility and survival, contributing to tumor angiogenesis [132], Sema-4D binds to its receptor Plexin-B1 on ECs to induce tumor angiogenesis [133], TP stimulates EC migration [134], uPA promotes ECM degradation and vascular invasion [135], and YKL-40 activates MAPK signaling in ECs, leading to increased expression of VEGFR-2 that facilitates vessel sprouting [136]. The gene discussed is KDR; the disease is neoplasm.