A potential mechanism behind such shift may be that oxidative stress and/or endothelial dysfunction result in eNOS uncoupling, which subsequently leads to the production of peroxynitrite, that is capable of inactivating PGIS thereby causing a shift in production from prostacyclin to TxA2 (Zou et al., 2004; Nie et al., 2006). This evidence concerns the gene NOS3 and endothelial dysfunction.