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Rivas et al went on to describe additional protective variants at IL23R, 21 and Stoll et al 22 showed DLG5 R30Q is a modest risk gene for CD.
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Sedentary work may be a modest risk factor.
However, many minor- or modest-risk genes are likely to be missed after adjustment of multiple testing.
We do not yet know whether improved understanding of intermediate risk and modest risk susceptibility genes will lead to similar medical utility.
Alternatively, large dnCNVs are found likely to contain multiple modest-effect risk genes.
Additional confirmation of these results and identification of additional genes conferring modest risk will lend further support to this model.
The huge amount of AD specific genetic data accumulated in the past decade also indicates involvement of multiple pathways wherein each gene confers only a modest risk.
The etiology of T2D, though not very clear, involves multiple pathways wherein each probable disease gene confers only a modest risk.
It could therefore be argued that our pathway-linked gene approach to identify modest risk loci, in combination with large scale GWAS, may be appropriate to ensure complete coverage of potential prostate cancer risk factors.
Polygenic models in which the existence of a large number of breast cancer susceptibility genes, each one conferring modest risk for developing the disease have been also proposed.
The familial clustering of T1D is explained by multiple common gene variants, each providing a modest risk but potentially associated to specific molecular mechanisms.
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