Furthermore, the study by Fang and colleagues10 has several significant limitations. On one level, their findings are merely hypothesis generating. Without specifically understanding how the presence of an elevated mPAP in the face of IPF causes PGD, it is difficult to simply accept these observations at face value. Moreover, the paucity of information about other hemodynamic variables, such as pulmonary capillary wedge pressure and pulmonary vascular resistance, makes it difficult to assess the true etiology for the elevation in mPAP. In an earlier analysis of PAH in IPF, investigators noted that patients with pulmonary hypertension had higher pulmonary capillary wedge pressures despite similar cardiac indices.8 Thus, was the higher incidence of PGD due to PAH or subtle left ventricular failure? It would not be surprising if underlying cardiac disease contributed to some of the authors’ results and simultaneously adversely altered outcomes. Despite the fact that transplantation centers generally do not list patients with significant left ventricular dysfunction, one cannot exclude the potential that some of the results described by Fang and colleagues10 arose in part from confounding due to cardiac disease or the development of mild left ventricular dysfunction between the time of listing and lung transplantation. Similarly, the sample size, although large for a prospective study in lung transplantation and IPF, was still relatively limited and further constrains our ability to draw generalizable conclusions.