Given that cd36, scd-1 and Fasn are overexpressed in our model and that their expressions are regulated by the nuclear receptors PPARγ for cd36[30] and LXR for scd-1 and Fasn[31], respectively, we suggest that the turn-over of activators of these nuclear receptors, i.e., fatty acid-derived ligands or cholesterol, might be affected in Pgp deficiency. Here, SCD is linked to hyperinsulinemic hypoglycemia, familial, 4.