Pharmacogenetics is the study of the effects of each individual genome on drug response. Information about genetic testing is now part of drug label as for abacavir, warfarin, clopidogrel, irinotecan, maraviroc, cetuximab, imatinib [1,2]. At present a wide range of drugs are employed for treating pathological conditions and chronic disorders, like cancer, diabetes, heart disease, etc. Ideally a drug is delivered so that it achieves a blood concentration that is within the therapeutic range: a too low drug concentration is ineffective, while one that is too high can be toxic. None of the drugs known to date proved to be 100% effective in every patient: the same dose of a given medicine may cause no response in some individuals, may produce the right therapeutic response in others, and may give rise to adverse responses in another part of them. These changes in the response may result from clinical differences between individuals (for example age or the presence of other pathological conditions), from diagnostic uncertainty, and from environmental factors. Besides, genetics has been proven to modulate in a significant way inter-patients variation in drug reaction. Genes are sequences of DNA that contain information determining the amino acid sequence of proteins, which participate in every cellular process, including drug response. Polymorphisms are DNA variations that occur at a frequency of 1% or greater, while DNA mutations occur less frequently than 1%: this definition is merely statistical and it does not reflect the functional role of both kind of genetic variants. In both cases in fact, if the DNA carries a sequence variation (a mutation or a polymorphism), the proteins may not be expressed properly, or not function correctly, or not reach the appropriate site of action. Regarding pharmacogenetics, individual genetic variations in enzymes of drug metabolizing enzymes, transporters, receptors, ion channels, target enzymes and signal transduction pathways, may lead to inadequate therapeutic responses. For example the genetic information of genes CYP2C9 (encoding a member of the cytochrome P450 superfamily of enzymes, which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids) and VKORC1 (encoding the enzyme which activates vitamin K) can assist in selection of the starting dose of warfarin [3] an anticoagulant which acts by inhibiting vitaminK-dependent coagulation factors. In particular, warfarin interferes with VKORC1enzyme, and DNA variants in CYP2C9 are related to differences in the drug’s clearance. The VKORC1 G1639A polymorphism is associated with lower dose requirements and increased bleeding risk, as well as inferior initial warfarin doses have been associated with the CYP2C9*2 and CYP2C9*3 variants [46]. Algorithms for genetics-based dosing have been developed and are available online (Online calculator for initiation of warfarin dosing based on pharmacogenetic algorithms, www.WarfarinDosing.org) [7]. The history of pharmacogenetics starts in 1957 when Arno