In this regard, inflammation plays a crucial role in the pathogenesis of NASH, which results from the infiltration of inflammatory chemokines and cytokines secreted by adipose tissues, Kupffer cells, and lipid‐laden hepatocytes during obesity, such as tumor necrosis factor‐α (TNF‐α), monocyte chemotactic protein‐1 (MCP‐1), and interleukin‐6 (IL‐6).2 The gene discussed is TNF; the disease is metabolic dysfunction-associated steatohepatitis.