This is a most instructive, delightful little book. First, the authors refresh the readers' understanding of the major health problem represented by pulmonary hypertension, emphasizing the important differences between the pulmonary and systemic circulation. They then clearly define the different forms of this syndrome, as accepted by the medical community in general and the WHO in particular, and summarize its epidemiology in a clear and rational way, subdividing the occurrence in function of unknown [idiopathic forms], known [caused by heart disease, pulmonary disorders or repeated thromboembolic events] or less defined multifactorial [hematologic, systemic or metabolic disorders] causes, with a focus on the often ignored occurrence in children. They then discuss the pathophysiology with the underlying remodeling of the pulmonary vascular wall, identifying major culprits: impaired protection by prostacyclin and nitric oxide and/or aberrant production of endothelin-1, apparently responsible for most idiopathic forms of pulmonary arterial hypertension. But they also stress how the syndrome can follow abnormal cardiac function (because of pressure overload in the pulmonary blood vessels) or chronic exposure to hypoxia [with the prominent role played by hypoxia-inducible (HIFs) and growth (VEGF)], insisting on the role of immune and inflammatory responses, not to mention their description of repeated pulmonary embolism. They masterfully describe the impact of the heightened pulmonary pressure on the right ventricle. Their chapter on mechanisms leading to vascular remodeling during pulmonary hypertension is a classical piece of rational scientific writing, elaborating in turn on altered ion channel activity (a most complex affair that they unravel clearly), perturbed interactions between endothelial and vascular smooth muscle cells (bringing nitric oxide and endothelin-1 back in the picture but not forgetting a long-time villain, serotonin), aberrant growth factor signaling and the facilitator role of hypoxia, the for most readers unknown contribution of extracellular vesicles, the emerging modulation by microRNAs, the importance of genetic and epigenetic modifications, as well as the potential contribution of signals from the adventitia (also a newcomer in vascular pathophysiology). The authors then move on to discuss in more details the causes underlying the excessive vasoconstrictor responses that accompany (cause?) pulmonary hypertension, discussing the failure of the nitric oxide pathway, the reduction in prostacyclin-production, the exaggerated production of endothelin-1 and the resulting activation of Rho-kinase signaling, the obvious deleterious role of reactive oxygen species, and the often unsuspected role of metabolic disturbances. The different chapters of this book not only will help the reader to appreciate the complexity of the multiple mechanisms that can lead to pulmonary hypertension, but also to understand much better the basis for the current therapeutic interventions. Although the authors undertake to address the cellular molecular mechanisms that underlie the occurrence of pulmonary hypertension, they do so with great clarity, with a wealth of most instructive and clear schematics, basing their writings on a thesaurus of references. This book is a must for anyone, whether basic scientist, clinical researcher or clinician interested in the major health problem represented by pulmonary hypertension. It also sets the stage for further exploration of the physiopathology and hence for the appropriate treatment of the syndrome.