DNMT1 and acute respiratory distress syndrome: Further bioinformatics analysis revealed that both TREs are highly conserved among eutherian mammals.[34] In a mouse brain injury model, short‐term administration of T3 reduced the expression levels of DNMT3a/3b and de novo DNA methylation.[35] These findings suggest that thyroid hormones and GC‐1 regulate the expression of DNMT families by binding to their receptors, indicating their potential epigenetic regulatory function in stress responses such as ALI/ARDS, in addition to their known roles as developmental epigenetic and transgenerational epigenetic modifiers.[36]