The inhibition of senescence by pirfenidone could be explained by the inhibition of β-catenin activation, as previous studies have suggested that Wnt/β-catenin TGF-β1 non-canonical pathway acts as a driver of cell senescence in IPF [48], and by inhibition of SBE activation, as activation of this DNA element response also increases the expression of the senescence markers, p21 and p16 [49]. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.