In particular, our study group has recently shown that AECIIs from IPF lungs are prone to apoptosis due to a thyroid hormone (TH) deficiency, and TH supplementation therapy attenuated experimental lung fibrosis and reversed morphological and functional mitochondrial abnormalities in AECIIs though mechanisms that involved induction of major transcription coactivators of mitochondrial biogenesis and effective mitophagy [13]. Here, TH is linked to tyrosine hydroxylase deficiency.