Table 1.

Summary of web based public databases and browsers of genetics/genomics tools

TnQTable 1What do we know?	What is still unknown?
Genetic variation plays a large role in asthma and allergic disease risk.	Identified variants account for a small proportion of disease and the factors that contribute to the majority of the heritability of allergic diseases are still unknown.
Non-SNP variation accounts for much more human genetic variation than single nucleotide diversity. Copy number variation regions (CNVRs) have been found in 12% of the genome.	The impact of structural variation (including CNV) on asthma and allergic disease is unclear. Furthermore, the technical and statistical assessment of CNVs is still evolving.
Whole genome information and high-throughout tools are now available for high-resolution mapping.	Linkage of genetic variation to phenotypic variation and to translation into biological function is still at infancy.
Gene-environmental interactions play an important role in allergic diseases and have been relatively well studied in model organisms.	Rigorous quantitative assessment of environmental influences will be necessary to elucidate gene-environment in humans.
Epigenetic effects on gene expression may persist even after the removal of the inducing agent, and can be passed on, through mitosis, to subsequent cell generations, constituting a heritable, epigenetic change.	Approaches to efficiently dissecting the role of gene-gene and gene-environment interactions, epigenetics, and imprinting are lacking
There are three main statistical approaches to identify disease associated genes:, association, and admixture mapping.	A positive association does not imply causality or a direct effect on gene expression or protein function
Recent evidence has revealed that rare alleles with major phenotypic effects can contribute significantly to common traits in the general population. Sequencing of candidate genes or entire genomes is currently the optimal way to identify rare variants.	The role of rare variants unclear, Furthermore, while genetic association and linkage studies are well suited to find common variants for common diseases, they are not optimal for identification of rare variants.
Recent evidence has revealed that rare/private SNPs can contribute significantly to common traits in the general population. While genetic association and linkage studies are well suited to find common variants for common diseases, they are not optimal for identification of rare variants. Sequencing of candidate genes or entire genomes is currently the optimal way to identify rare variants.	Although rare and private SNPs are largely unknown, the 1000 Genomes Project, a deep-resequencing project will provide detailed genetic variation data on over 1000 genomes from 11 populations around the world.
Novel approaches to capture human genetic variation have integrated expression global gene expression arrays, DNA sequence variation arrays, and public databases. Variation in gene expression is an important mechanism underlying susceptibility to complex disease. An integrated genetic/genomic approach allows the mapping of the genetic factors that underpin individual differences in quantitative levels of expression (expression QTLs; eQTLs).	Genetic studies have identified hundreds of genetic variants associated with complex human diseases including 43 replicated genes for asthma. The variants identified so far confer relatively small increments in risk, and explain only a small proportion of disease heritability. The clinical implications, i.e., the contribution of the genetic variation to asthma subphenotypes, variations in treatment response, and different disease outcomes remain largely undetermined.