Oxidized LDL inhibited GTPCH1 gene expression in interleukin‐1 beta activated vascular smooth muscle cells, which was postulated that diminished availability of BH4 may additionally impair the generation of NO in atherosclerosis.25 Macrophage‐specific GTPCH1 deficiency resulted in increased foam cell formation and altered cellular redox signalling, with decreased expression of antioxidant genes and increased reactive oxygen species in the atherosclerotic mice model.26 Thus, GTPCH1 plays an important protective role in the cardiovascular diseases such as atherosclerosis. This evidence concerns the gene GCH1 and cardiovascular disorder.