Dissatisfaction has been voiced over recent decades concerning the lack of a relevant cardiovascular disease (CVD) scoring system for European populations. Recently this deficiency has been repaired with the publication of SCORE,1 although nonfatal events are still not catered for. In addition, the entire sequence of the human genome has recently been published.2 Common chronic diseases, such as coronary heart disease (CHD) and stroke, may have a strong genetic component. They are, however, caused not by a single genetic defect but by the interactions of many genetic and environmental factors. Hence, they are often called complex, multifactorial diseases. Moreover, the biological effects of common genetic variants are likely to be small in magnitude; indeed, variants with large biological effects tend to be rare, for example familial hypercholesterolaemia. Investigators examining the genetic background of complex, multifactorial diseases should, therefore, realize that they are looking for interactions between genetic variants with small, or at most moderate, effects. It is obvious that the reliable detection of these effects requires large sample sizes and abundant statistical power, which can be achieved only in a large collaborative study using high-throughput genotyping. It should be emphasized, however, that moderate and even small effects can carry considerable public health significance if the genetic variants in question are common in the population. The remarkable success of the Human Genome Project has been possible only through the multinational collaboration of several research laboratories and the open exchange of information through the Internet. Developments in genetics open up new possibilities for the prevention and treatment of chronic diseases, but to capitalize on this potential, a better understanding of the significance of genetic variation and the interactions of genetic variants with environmental factors is needed.