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. The gene discussed is CYP4F2; the disease is Stroke.