ABCG5 and sitosterolemia: The mechanism underlying the association between the other variants and cholesterol levels is still unknown; however, Graf, et al. [32] analyzed 13 sitosterolemia-causing ABCG5/G8 mutations and found that all the mutations reduced G5/G8 heterodimer trafficking from the endoplasmic reticulum to the Golgi apparatus and that 10 of them prevented stable heterodimer formation between G5 and G8.