Pharmacogenomics| Gene | Drug | Clinical consequence |
| Drug metabolism |
| NAT-2 | Isoniazid, hydralazine, procainamide, sulfonamides | Neuropathy, lupus erythematosus |
| CYP2D6 | Beta-blockers, antidepressants, codeine, debrisoquine, antipsychotics, many others | Arrhythmias, dyskinesia with antipsychotics, narcotic effects, changes in efficacy, many others |
| CYP2C9 | Tolbutamide, phenytoin, nonsteroidal anti- inflammatories | Anticoagulant effects of warfarin modified |
| RYR-1 | Halothane and other anesthetics | Malignant hyperthermia |
| Protection against oxidants |
| G6PD | Primaquine, sulfonamides, acetanilide, others | Hemolytic anemia |
| Drug targets |
| ACE | Captopril, enalapril | Modified response to treatment of cardiac failure, hypertension, renal disease |
| HERG | Quinidine | Cardiac arrhythmia (long Q-T syndrome) |
| HKCNE2 | Clarithromycin | Drug-induced arrhythmia |
Source: Modified from Evans and Relling (Science 286: 487 [2001], as quoted in WHO 2002a).
Note: Table shows examples of genetic polymorphisms that cause unwanted effects of drugs or modification of response. Currently, arrays are being developed for the rapid identification of families of polymorphisms related to infection-defense genotypes, drug-metabolism genotypes, and many others. Although many polymorphisms associated with variations to drug response or toxicity have been defined, the bulk of variation of response to drugs follows a multifactorial pattern of inheritance.
The examples shown are as follows: NAT-2 = N-acetyltransferase; CYP = cytochrome P450; RYR-1 = ryanidine receptor; G6PD = Glucose-6-phosphate dehydrogenase; and ACE = angiotensin-converting enzyme. HERG and HKCNE2 are potassium channels.