Animal studies also showed that mice with ABCG5/G8 deficiencies may cause hypertriglyceridemia via multiple metabolic pathways [27] and that sterol transportation via ABCG5 and ABCG8 opposes the development of fatty liver disease and loss of glycemic control independently of phytosterol accumulation [28]. This evidence concerns the gene ABCG8 and hypertriglyceridemia.