Several mechanisms have been reported, including hypercontraction of coronary smooth muscle,10 enhanced autonomic nervous system activity,11,12 endothelial dysfunction, and increased oxidative stress.13 Vasospasm can be triggered by decreased availability of nitric oxide (NO) in the endothelium,13 and genetic risk factors for VSA have been reported in genes encoding NO synthase.14 Very recently, a Japanese group published a short report15 investigating the association of the RNF213 p.R4810K variant with 66 cases of VSA. The gene discussed is RNF213; the disease is endothelial dysfunction.