By limiting confounders affecting plasma CNP peptides (such as cardiovascular risk in healthy subjects), variable renal function (correcting for serum creatinine), and variable cardiac status in subjects with overt CAD (measuring plasma BNP and correcting for BNP cross reactivity in the CNP assay), the findings clearly set a limit on the putative actions of statins on CNP production within the healthy and diseased vasculature. This evidence concerns the gene NPPB and coronary artery disorder.