In particular, we have observed that SB3 overexpression not only leads to increased fibrosis, as previously reported (31), but also to an increase in transcript levels for TNFα and IL-1β and to recruitment of infiltrating monocyte-derived macrophages that accumulate mainly in crown-like aggregates, a feature which is characteristic of human advanced NAFLD (42, 43). The gene discussed is TNF; the disease is metabolic dysfunction-associated steatotic liver disease.