demonstrated a correlation between serum Hcy levels and hepatic inflammation and fibrosis in nonalcoholic steatohepatitis, with knockout of the CBS gene leading to Hcy accumulation and exacerbating NASH progression.[13] In addition, Fol is undoubtedly an essential factor in decreasing plasma Hcy level, and could be applied in the treatment with diseases correlated with HHcy.[14, 15] However, the impact of altered Hcy metabolism in AT2 cells on pulmonary fibrosis, as well as the protective role of Fol in IPF, remains largely unknown, and the underlying mechanisms are yet to be elucidated. The gene discussed is CBS; the disease is pulmonary fibrosis.