ACTA1 and idiopathic pulmonary fibrosis: The effects of UCP2 silencing on cellular reprogramming were primarily explained by effects on senescent myofibroblasts which express higher basal levels of α‐SMA and COL1a1 (Figure S5b); a similar effect on the downregulation of these pro‐fibrotic markers was also observed with treatment of IPF myofibroblasts with a pharmacological inhibitor of UCP2, genipin (Zhang et al., 2006) (Figure S5c,d).