Genetic factors are implicated in atherogenesis by family and twin studies of coronary artery disease, interacting with the environment to produce the phenotypic disease. Restriction fragment length polymorphisms provide useful linkage markers with which to study the genetics of this disease, the effectiveness of marker loci being characterized in terms of their polymorphism information content. Other forms of nucleotide variation, including variable number of tandem repeats can also provide linkage markers for aetiological loci and can be detected by the use of polymerase chain amplification followed by sequencing, denaturing gel electrophoresis, base pair specific chemical cleavage or the use of oligonucleotide probes. Linkage markers may be used either in population association or familial studies. Candidate genes may be studied or complete genomic mapping attempted. A review of potential candidate genes for atherosclerosis is presented.