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In summary, many complex traits are driven by enormously large numbers of variants of small effects, potentially implicating most regulatory variants that are active in disease-relevant tissues. To explain these observations, we propose that disease risk is largely driven by genes with no direct relevance to disease and is propagated through regulatory networks to a much smaller number of core genes with direct effects. If this model is correct, then it implies that detailed mapping of cell-specific regulatory networks will be an essential task for fully understanding human disease biology. - www.cell.com