In the present study, we found that CSAD is downregulated in the NAFLD model, and further results have shown that CSAD overexpression can alleviate NAFLD-associated pathologies, including body weight, liver/body weight ratio, hepatic triglyceride and total cholesterol, and the degree of steatosis, probably by improving mitochondrial injury in HFD mice. The gene discussed is CSAD; the disease is metabolic dysfunction-associated steatotic liver disease.