Consistently, excessive lipid accumulation could further promote TLR4/NF‐κB signaling to trigger the leakage of proinflammatory cytokines (TNF‐α, IL‐6, IL‐1β, and IL‐18), thus exacerbating the vicious cycle of inflammatory responses in the liver to aggravate fatty liver progression (Fei et al. 2020). The gene discussed is IL18; the disease is Hepatic steatosis.