The results showed that ATL-3 was able to reverse the effects of Nrf2 interference on lung fibrosis injury, ameliorate bleomycin-induced pulmonary fibrosis and oxidative stress, and enhance survival by modulating the Nrf2/NQO1/HO-1 signaling pathway and decreasing the expression of apoptosis-related proteins (caspase-3/9), TGF-β, α-SMA, and inflammatory factors (42). Here, CASP3 is linked to pulmonary fibrosis.