There is a complex interaction between inflammation, degradation of extracellular matrix components, neovascularization of the plaque, and the presence of comorbidities such as diabetes or chronic kidney disease.[37] Most of the plaques from our stroke patients were calcified, but this is partially explained by the increased frequency of homozygous and heterozygous genotypes of VKORC1 and CYP4F2 polymorphisms. This evidence concerns the gene CYP4F2 and stroke disorder.