In the pathogenesis of MASH, studies have found that a lack of receptor-interacting protein kinase 3 (RIPK3) leads to the upregulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) and fibroblast growth factor 21 (FGF-21) to realize the reverse recovery of MASH [47]. This evidence concerns the gene RIPK3 and metabolic dysfunction-associated steatohepatitis.