We therefore propose the following testable hypothesis: IGF-2 contributes to pulmonary vascular remodeling and right-ventricular adaptation in PAH via IGF-1R/IR-mediated activation of PI3K/Akt and MAPK pathways, in a cell-type- and time-dependent manner (Blyth et al., 2020; Liu et al., 2001). The gene discussed is AKT1; the disease is pulmonary arterial hypertension.