This is based on our observations of decreased FA consumption in IPF myofibroblasts expressing high levels of UCP2, an effect that was reversed with UCP2 silencing, detected by both mass spectrometry and lipid staining approaches; furthermore, increased basal oxygen consumption in these UCP2‐silenced cells was abrogated with etomoxir, an inhibitor of CPT1a, the rate‐limiting enzyme for FAO. Here, UCP2 is linked to idiopathic pulmonary fibrosis.