Furthermore, in a model of non-alcoholic steatohepatitis, overexpression of clusterin has been shown to inhibit pro-inflammatory cytokine production (e.g., TNF-α and IL-1β) and hepatic macrophage infiltration, and to abolish hepatic fibrogenesis through the activation of the transcription factor Nrf2 which activates the antioxidant response element (Park et al., 2018), thus increasing proteins that lead to detoxification and elimination of reactive oxygen species and electrophilic agents (Falgarone and Chiocchia, 2009; Nguyen et al., 2009). The gene discussed is TNF; the disease is metabolic dysfunction-associated steatohepatitis.