The antifibrotic potential of hesperidin is mediated through the inhibition of TGF-β1/Smad3/AMPK and IκBα/NF-κB pathways which ameliorate the modulation of oxido-inflammatory markers (Nrf2 and HO-1) and pro-inflammatory markers (TNF-α, IL-1β, and IL-6) to reduce collagen deposition during pulmonary fibrosis (Figure 1(Fig. 1)). This evidence concerns the gene SMAD3 and pulmonary fibrosis.