Furthermore, we had originally demonstrated that WD/FG significantly increased mRNA levels of Gal, Galr1, Galr2, and Galr3 in mouse heart ventricles compared to those in negative controls in our experiments, suggesting that other members except for GalR2 might play a role in cardiovascular physiology and pathophysiology related to metabolic diseases. The gene discussed is GAL; the disease is Other metabolic disease.