This kind of activity, by affecting Smad proteins, was proven, e.g., for apolipoprotein A1 [48], plant-derived hesperidin, paeoniflorin, and celasterol [49,50,51], as well as for two drugs approved in the treatment of idiopathic pulmonary fibrosis, nintedanib and pirfenidone [52,53]. This evidence concerns the gene APOA1 and pulmonary fibrosis.