RAF1 and pulmonary fibrosis: In conclusion, WEL can decrease the associated inflammation by attenuating Raf1-MAPKs signaling pathway to inhibiting inflammatory cytokines production, and increase the activation of AMPK in the BLM-induced pulmonary fibrosis models, preventing an increase in pro-fibrotic markers such as Col I and α-SAM and attenuating a decreasing in anti-fibrotic marker such as E-cadherin.