Pharmacogenetics is the variability of drug response due to inherited chara
cteristics in individuals. Drug metabolizing enzymes have been studied for
decades, first as chemical reactions and, more recently, as specific polymo
rphisms of known molecules. With the availability of whole-genome single-nu
cleotide polymorphism (SNP) maps, it will soon be possible to create an SNP
profile for patients who experience adverse events (AEs) or who respond cl
inically to the medicine (efficacy). Proof-of-principle experiments have de
monstrated that high density SNP maps in chromosomal regions of genetic lin
kage facilitate the identification of susceptibility disease genes. Whole-g
enome SNP mapping analyses aimed at determining linkage disequilibrium (LD)
profiles along an ordered human genome backbone are in progress. SNP 'fing
erprints' or SNP PRINTssm will be used to identify patients at greater risk
of an AE, or those patients with a greater chance of responding to a medic
ine. As LID maps for various ethnic populations are constructed, the number
of SNPs necessary to measure for an individual will decrease. Standardized
pharmacogenetic maps for drug registration and post-marketing surveillance
will result in safer, more effective and more cost-efficient medicines. Th
e timing of these pharmacogenetic applications will occur over the next 5 y
ears. In contrast, the benefits of pharmacogenomic applications such as the
identification of new tractable targets will not be visible as new medicin
es for 7-12 years, due to the lengthy drug development and registration pro
cesses.