The genetic deletion of β3 integrin (Itgb3) results in increased angiogenesis and tumor growth [39], while antibody targeting of αvβ3/β5 integrins or mutations of a tyrosine phosphorylation site that leave the β3 receptor intact but disrupt downstream signaling suppresses angiogenesis and tumor growth, suggesting a similar antagonistic effect [40]. This evidence concerns the gene ITGB3 and neoplasm.