Notably, expression of ENO1, PDIA3 and T1α decreased upon inhibition of Wnt/β-catenin signaling (a pathway that is involved in impaired alveolar epithelial cell repair in vitro and in vivo and is suggested as a potential therapeutic target for pulmonary fibrosis) during ATII-to-ATI trans-differentiation, whereas CBR2 levels were stabilized. The gene discussed is PDIA3; the disease is pulmonary fibrosis.