Combining this piece of evidence with the fact that heart disease implies an underlying inflammatory phenotype [32] and that vitamin K has an anti-inflammatory role on macrophages [3] we hypothesize that one of the mechanisms through which VKORC1 and CYP4F2 polymorphisms interact with ischemic heart disease is by enhancing an already existing inflammatory environment. This evidence concerns the gene CYP4F2 and coronary artery disorder.