LOX was also shown to be essential in endothelial cells in vitro and in angiogenesis in vivo by activating AKT through PDGFRβ stimulation, resulting in increased VEGF expression, a mechanism characterized in models of both colorectal cancer and breast cancer, and supported by clinical correlations between LOX, VEGF levels and blood vessel formation in colorectal tumors [22]. The gene discussed is LOX; the disease is breast cancer.