During NAFLD/NASH, reactive oxygen species and damage-associated molecular patterns released from injured hepatocytes undergoing apoptosis or necrosis trigger macrophages secrete a variety of chemokines to recruit monocytes and other leukocytes, leading to insulin resistance and oversecretion of proinflammatory and chemokines such as TNF-α, IL-6, IL-1β, and MCP-1 (64). This evidence concerns the gene TNF and metabolic dysfunction-associated steatohepatitis.