In COPD+NAFLD, the baseline metabolic milieu—characterized by hyperinsulinemia, elevated free fatty acids, and hepatic inflammation—likely sustains high EGR1 expression via MAPK/ERK and NF-κB activation, compounded by disruption of the liver-specific HNF4α/SHP regulatory axis. This evidence concerns the gene EGR1 and metabolic dysfunction-associated steatotic liver disease.