However, when MASLD remains unresolved in the long-term, TNF-α maintains a longitudinal intra-hepatic inflammation, contributes to hepatic fibrosis, and perpetuates the activation of proapoptotic and protumorigenic pathways [e.g., mitogen-activated protein kinases (MAPK), c-Jun N-terminal kinase (JNK), caspase-8], which eventually outweigh the initial beneficial effects [21]. The gene discussed is TNF; the disease is fibrosis.