Mechanistically, PERKα treatment upregulated the expression of genes such as Atf3, Ddit3, and Gdf15, and induced an increase in serum GDF15 levels, potentially contributing to reduced food intake.[73,74] These observations suggest that short-term PERKα treatment may enhance metabolic homeostasis and offer a preventive approach against the development of NAFLD. The gene discussed is GDF15; the disease is metabolic dysfunction-associated steatotic liver disease.