In NASH models, molecular hydrogen reverses hepatic fibrosis by inhibiting the phosphorylation of signal transducer and activator of transcription 3 (STAT3), the activation of downstream mitogen-activated protein kinase (MAPK) signaling, and regulating oxidative stress–inflammatory pathways (e.g., nuclear factor-κB [NF-κB]), thereby reducing hepatic stellate cell activation and collagen deposition [30]. This evidence concerns the gene STAT3 and metabolic dysfunction-associated steatohepatitis.