For instance, a previous study has shown that an excess concentration of hepatic CXCL1 leads to an oxidative stress response, as indicated by the increased activation of stress kinases such as apoptosis signal-regulating kinase 1, which accelerates the nonalcoholic steatohepatitis progression (Hwang et al., 2020). This evidence concerns the gene CXCL1 and metabolic dysfunction-associated steatohepatitis.