In addition to disease-associated SNPs, GWAS studies of recent years have also provided evidence that SNPs are not randomly distributed in the genome, but tend to be overabundant in specific regions of linkage disequilibrium (LD). In previous studies (Preuss et al. 2011, Riemenschneider et al. 2012), we were able to show that evolutionarily driven processes have a genome-wide influence on the genetic predisposition to complex diseases. For this purpose, we analyzed the genome-wide distribution of disease-associated SNPs based on data from the pilot phase of the 1000 Genomes Project, a set of publicly available GWAS data, and meta-analyses for three of the four HapMap populations (CEU, AFR, ASN). We observed a specific accumulation of disease-associated SNPs in regions of pronounced LD, which contain genes with functions in the immune system. Detailed analyses also revealed strong signals of so-called selective sweeps for disease-associated variants in regions with a concentration of immune defense genes. Interestingly, disease-associated SNPs are more frequently observed in populations under selective pressure than in populations not subject to such evolutionary selective pressure. Our data indicate that continuous selective pressure over the course of evolution has altered the genomic architecture of the human genome such that immunity genes cluster in specific genomic regions. In this process, disease-associated variants also accumulate disproportionately via genetic hitchhiking , which then contribute to the genetic predisposition for complex diseases, such as type 1 diabetes or rheumatoid arthritis, but also coronary heart disease. These findings formed the basis for a further study in 2013 on the role of a pro-inflammatory predisposition in the etiology of coronary heart disease from a systems biology and evolutionary biology perspective. In a comprehensive bioinformatics analysis, including GWAS data from the NHGRI GWAS database, as well as results from a study in cooperation with the Institute of Immunology (Prof. Johannes Roth) at the University Hospital Münster, in which we generated specific SNP, methylation, and expression data in human, LPS- and MRP8-stimulated monocytes, we were able to demonstrate the existence of a molecular network that includes both cardiovascular and inflammatory risk genes, and that this interaction network is under selective pressure. These results provide first insights into the molecular structure of inflammatory vascular diseases and a direct molecular link between systemic inflammation and increased cardiovascular risk.