A potential mechanism of action for MMT has been elucidated in the bleomycin and TGF-β induced pulmonary fibrosis in vivo models, where the lung myofibroblasts induced epigenetic modifications in the tissue macrophages via histone lactylation, skewing the polarization of the alveolar macrophages into the pro-fibrotic phenotype [129]. The gene discussed is TGFB1; the disease is pulmonary fibrosis.