H yperplasia of pulmonary artery SMCs (PASMCs) is a pathological hallmark of pulmonary arterial hypertension (PAH). In this issue of the JCI, McMurtry et al. report that adenovirus-mediated overexpression of survivin — a multipotent inhibitor of apoptosis — induces PAH in rats, whereas inhalation of an adenovirus vector encoding a mutant survivin gene with dominant-negative properties reverses established monocrotaline-induced PAH. These findings raise important issues regarding the role of survivin in the pathogenesis of PAH, its value as a prognostic indicator, and its use as a target for new therapeutic strategies.