FOSL2 and pulmonary fibrosis: Studies have shown that BACH1 suppression relieves fibrosis and inflammation by blocking the ERK signaling.[423] BACH1 transcriptionally enhances FOSL2, thereby inducing the M2 macrophage phenotype through activating the TGFβ/SMAD signaling to facilitate the transformation of lung fibroblasts into myofibroblasts, and BACH1 deficiency alleviates BLM‐mediated pulmonary fibrosis.[424] These studies suggest that BACH1 seems to be detrimental in lung fibroblast cells, and inhibition of BACH1 can alleviate pulmonary fibrosis.