In experimental monocrotaline (MCT)-induced PAH in rats, morphological and functional skeletal muscle changes were related with impaired exercise capacity, including smaller muscle fiber cross-sectional area (CSA), decrease in contractile function and upregulation of pro-atrophic ubiquitin ligases (Fbx32, Trim63) which contributed to proteolysis, compared to control rats [6, 7]. The gene discussed is FBXO32; the disease is pulmonary arterial hypertension.