We hypothesized that cystatin C may exert GFR independent effects increasing the risk of coronary artery disease (CAD) and thus set out to test whether or not there is a causal relationship between cystatin C and risk of CAD using a Mendelian Randomization approach where the strongest genetic signal for plasma concentration of cystatin C identified thus far (rs13038305) was related to risk of CAD. The gene discussed is CST3; the disease is coronary artery disorder.