The hypotheses were generated by the findings from Luan et al. [17] seem to support the findings by Kim et al. [18], showing that GDF15 downregulates the expression of genes involved in the development of liver fibrosis and that the overexpression of GDF15 in transgenic mice alleviates hepatic inflammation and the NASH phenotype [18]. This evidence concerns the gene GDF15 and metabolic dysfunction-associated steatohepatitis.