Genetic susceptibility to asthma is due to multiple genes that interact with each other and the environment. There are many known environmental influences, such as viral and other respiratory infections and exposure to allergens, air pollutants, and active or passive cigarette smoke (1). Genome-wide screens for asthma and atopy have been completed and show statistical evidence for linkage in different racial groups and population samples (4, 5). Some of these linkages have already been replicated in different studies, and most of them are in chromosomal regions containing relevant candidate genes that may regulate inflammatory processes including cytokine synthesis, T-cell responses, or other immune functions. These associations support the relevance of this genetic approach in understanding susceptibility to and expression of asthmatic and allergic phenotypes. Once specific sequence variants are identified, it will become important to test for gene-environment interaction in order to understand the significance and relative effect of each gene on the overall phenotype.