Considering the beneficial effects of the ACE2‐Ang1‐7‐Mas1 system and the counterregulatory role in opposing the classing RAS, this may provide another potential mechanism for the observed improvement in cardiac hypertrophy and sodium handling in RGZ‐treated CHF rats.49 In support of this notion of dual and perhaps interdependent regulation of both effectors, a previous study from our laboratory found increased cardiac ACE/ACE2 protein abundance and activity ratio in rats with ACF‐induced CHF.50 The gene discussed is MAS1; the disease is cardiac hypertrophy.