Overall, this evidence confirms the involvement of these inflammatory mediators in NAFLD development, suggesting that OA-induced lipid accumulation can be considered a useful in vitro model for studying the reduction in the lipid accumulation in response to a natural extract, leading to increased levels of ROS and expression of TNF-α, IL-1α, IL-1β, MCP-1 and G-CSF [101]. Here, IL1B is linked to metabolic dysfunction-associated steatotic liver disease.