However, although our mouse model of breast cancer did not demonstrate a significant change in p-AKT protein level or ETA receptor (Figures 4B and 4D), atrasentan significantly decreased p-AKT protein levels in the heart tissues (Figures 4B and 4D), suggesting that atrasentan significantly blocked the endothelin signaling in our breast cancer–injected mice. The gene discussed is AKT1; the disease is breast cancer.