Collectively, these observations suggest that endothelial cells within breast cancer might function as a CSC niche by providing Jag1 to the Notch1 receptor expressed in neighboring breast CSCs to elevate Zeb1 expression, which in turn reciprocally leads to the upregulation of endothelial Jag1 in a VEGFA-dependent paracrine fashion. This evidence concerns the gene ZEB1 and breast cancer.