Investigation using vascular smooth muscle cell-specific Gch1 deletion (e.g. SM22-cre mice) mice or knockout of Gch1 in both endothelial cells and vascular smooth muscle cells may provide an insight into understanding the role of Gch1 and BH4-dependent NOS regulation in different vessel wall cells in the pathophysiology of LPS-induced endotoxaemia and septic shock. The gene discussed is GCH1; the disease is septic shock.