These findings are in concordance with previous reports demonstrating that overexpression of the activated Notch4 oncoprotein in normal breast epithelial cells abrogated their normal morphogenesis in 3D culture.43 Furthermore, knockdown of Notch4 in MCF-7 cells completely abolished their ability to form tumors in the mouse mammary fat pad.44 Overall, the results described above suggest that Int-αvβ3 expression in CLPslow will promote their differentiation into acinar-like organoids via downregulation of Notch4 expression and downstream signaling, thus inhibiting tumor growth. This evidence concerns the gene INTU and neoplasm.