Furthermore, adropin knockout (AdrKO) exacerbated hepatic steatosis, inflammation, and fibrosis, while adropin treatment alleviated these conditions by promoting the expression of Gclc, Gclm, and Gpx1, as well as increasing glutathione (GSH) levels in an Nrf2-dependent manner, thereby preventing NASH progression in mice (10). The gene discussed is NFE2L2; the disease is metabolic dysfunction-associated steatohepatitis.