In addition to rare co-segregating variants, GWAS have implicated common risk-conferring variants and FBN1, LRP1, PHACTR1, ECM1, ADAMTSL4, LINC00310, C1orf54, MRPS21, and AFAP1 as candidate genes for SCAD [4,5,6], highlighting the heterogeneity of the disorder. This evidence concerns the gene C1orf54 and spontaneous coronary artery dissection.