We are tempted to speculate that the delayed onset of EndMT could result from the activation of Slit2 and its receptors’ ROBO1–ROBO4-dependent signaling in the 1st week of breast cancer progression (Fig. 6), since Slit2 was previously reported to inhibit both TGF-β [40] and Snail [41] signaling, both involved in the triggering of mesenchymal transformation of endothelial cells [20, 22–25, 34]. This evidence concerns the gene SLIT2 and breast cancer.