Recent studies have demonstrated that overexpression of CXCL1 or IL-8 can induce hepatic neutrophil infiltration and promote the progression of fatty liver to NASH in high-fat diet (HFD)-fed mice, which is mediated via the p47Phox-dependent production of ROS by neutrophils.155 Neutrophils can release neutrophil extracellular traps (NETs) to control infection, and in humans, elevated NET markers in serum are associated with NASH severity; similarly, reducing NET release improves liver inflammation and NASH-related HCC in mouse models.234. This evidence concerns the gene CXCL8 and metabolic dysfunction-associated steatohepatitis.