The association between SNPs in LPA gene and circulating Lp(a) levels, and consequently with CHD, may be mediated by various mechanisms: (i) some of the SNPs may be in linkage disequilibrium with the KIV-2 repeat polymorphism which has been shown to explain approximately 50% of the genetic variation in Lp(a) concentrations; (ii) certain SNPs may directly influence the transcriptional and/or translational processes of the LPA gene (Paultre et al., 2000); and (iii) some non-causal SNPs may be in linkage disequilibrium with SNPs having causal effect on Lp(a) concentrations. This evidence concerns the gene LPA and coronary artery disorder.