Our study predicts HNF4A to be highly activated in the SPI-fed rats, along with the upregulation of several CYPs and apolipoproteins (Figure 5), which could be exerting a protective influence against lipid accumulation in the liver tissue; thus, preventing inflammation and the progression to NAFLD in the long-term. The gene discussed is HNF4A; the disease is metabolic dysfunction-associated steatotic liver disease.