The aim of this study was to verify that chronic treatment with the PRMT3 inhibitor SGC707 would inhibit hepatic triglyceride synthesis and the development of non-alcoholic fatty liver disease and, as a result, decrease the plasma hyperlipidemia extent and atherosclerosis susceptibility in Western diet-fed LDL receptor knockout mice. This evidence concerns the gene LDLR and metabolic dysfunction-associated steatotic liver disease.