In addition, the mechanisms by which Mfn1iΔAEC2 or Mfn2iΔAEC2 mice are more susceptible to bleomycin may not fully explain the development of spontaneous fibrosis in the Mfn1/2iΔAEC2 mice, with Sftpc expression reduced in Mfn1- or Mfn2-deficient AEC2 cells in bleomycin-induced lung fibrosis, but remaining unchanged in Mfn1/2-deficient AEC2 cells. The gene discussed is MFN2; the disease is pulmonary fibrosis.