Given that: 1) breast cancer cells secrete endothelin(ET)-1 to stimulate tumor growth;10 2) endothelin receptor type A (ETAR) is highly expressed in both cancer cells and cardiomyocytes;11, 12, 13, 14 3) activation of the endothelin system is known to contribute to cardiac remodeling and heart failure pathogenesis;11, 12, 13, 14 and 4) inhibition of endothelin signaling lessens heart failure and cardiac hypertrophy,15, 16, 17 we postulated that shared signaling pathways perpetuate endothelin axis activation in both systems. The gene discussed is EDNRA; the disease is cardiac hypertrophy.