These KI data support earlier findings in healthy people with GP.Mur—lower fractional exhaled NO (FeNO), lower FMD (rather due to stronger RBC scavenge of NO metabolites than endothelial defects), higher blood pressure, and stronger dependence of FMD and BP on individual Hb levels.27–29 Though both GPMur KI and eNOS knock-out present similar phenotypes—lower NO bioavailability and hypertension,63 their sites of action and mechanisms are different. This evidence concerns the gene GSTM1 and Hypertension.