CXCL1 and metabolic dysfunction-associated steatohepatitis: We further revealed that IL-22 could mitigate Cxcl1 overexpression-induced liver injury in HFD-fed mice through a mechanism that required the induction of the antioxidant enzymes metallothionein-1 and metallothionein-2, thereby suggesting that attenuation of oxidative stress could ameliorate neutrophil-driven experimental NASH.