demonstrated, using a CSC KO model for NRP1 or VEGF-A, that this signaling axis was necessary to ensure the specific traits of CSCs in vitro and in vivo, and that the VEGF-A/NRP1 axis conferred the strain phenotype to breast cancer cells by activating the WNT/β-catenin signaling pathway (108). The gene discussed is NRP1; the disease is breast cancer.