This notion is further substantiated by the above-mentioned study on CXCL1-induced NASH (65), which provides several lines of evidence that neutrophils promote NASH development through production of ROS that activate several stress kinases (ASK1, p38/JNK-CASP3 pathway) in the liver, resulting in liver injury, inflammation and fibrosis. This evidence concerns the gene MAP3K5 and metabolic dysfunction-associated steatohepatitis.