Hepatocyte injury is the key feature that differentiates NASH from isolated steatosis.32 Injured hepatocytes release factors promoting the accumulation of immune cells that produce hepatotoxic substances and induce further injury and inflammation.33, 34 In our study, the genes involved in the Toll‐like receptor signaling pathway, the NF‐κB signaling pathway, the NOD‐like receptor signaling pathway, and TNF signaling pathway were significantly increased in the NASH rat models. Here, NFKB1 is linked to steatosis.