Previous studies have demonstrated that the expression of AKT1 is elevated in IPF patients and that a reduction in the production of AKT1 significantly reduces the secretion of α-smooth-muscle actin (α-SAM) and fibronectin, as well as inhibiting the progression of TGF-β-induced PF (Nie et al. 2019; Abdalla et al. 2015). The gene discussed is AKT1; the disease is idiopathic pulmonary fibrosis.