These data on αSMA expression conflict with animal models of fibrosis, which suggest that pirfenidone and nintedanib decrease myofibroblast accumulation and differentiation, but are in keeping with the most recent histopathological results from IPF patients treated with either nintedanib and pirfenidone, where both drugs failed to reduce the density of the pathognomonic fibroblast foci (Zhang et al., 2019). This evidence concerns the gene ACTA1 and idiopathic pulmonary fibrosis.