IGFBP-2 may contribute to the pathogenesis of PAH through several mechanisms, including the stimulation of cellular growth via non-IGF-dependent pathways, its association with inflammation-related cardiorespiratory disorders, and its regulation of phosphatase and tensin homolog (PTEN) in vascular smooth muscle cells (Yang et al., 2020). The gene discussed is PTEN; the disease is pulmonary arterial hypertension.