We can hypothesize that in healthy humans, high levels of GR and HNF4α lead to high hepatic basal expression of CXCL2 and induction of CXCL2 in early inflammatory liver diseases, whereas patients with late-stage hepatic diseases have a deficiency of HNF4α and GR, leading to the decreased CXCL2 levels observed in patients with AH, nonalcoholic steatohepatitis, and liver cancer. The gene discussed is HNF4A; the disease is liver disorder.