Some research suggests that IGF-1 is involved in the pathophysiology of PAH, with its dysregulated signaling contributing to pulmonary vascular remodeling, smooth muscle cell proliferation, and fibrosis, ultimately exacerbating the disease (Cao et al., 2000; Sun et al., 2016; Bouzi et al., 2021). This evidence concerns the gene IGF1 and pulmonary arterial hypertension.