The right ventricle (RV) of the heart, which pumps blood through a low pressure, low resistance “lesser” circulation, is now receiving more attention by researchers and clinicians, after many years of benign neglect.[1–7] Some of the many reasons for neglecting the RV assumed that (1) In the context of global cardiac performance, the RV was not very important; and (2) The cellular and molecular mechanisms of RV failure (RVF) were not different from those responsible for LV failure. Perhaps the biggest knowledge gap originated from the lack of experimental studies modeling the development of RVF, and from attempts to extrapolate mechanisms of chronic RVF from studies originally designed to study acute RVF. These likely explain why “pressure overload” is the most frequent—and sometimes exclusively—quoted mechanism of RVF. Indeed, patients with chronic, progressive pulmonary vascular disease most frequently die of RV failure.[8,9]However, as we enlarge our knowledge of in the pathobiology of RVF, we should also begin to consider RVF as a “progressive,” but not necessarily “chronic,” phenomenon.