Figure 1
Figure 1. The utility of intermediate traits as end points. This greatly simplified schematic assumes there are 10 genes contributing equally to the clinical end point (ie, 10% each, faint dashed lines). Another level of complexity to the pathophysiology is superimposed by including 5 intermediate traits, each contributing 20% to the clinical outcome. In this example, genes 1 and 2 have a much larger effect on platelet reactivity (50%) than on the clinical end point (10%). Of course, environmental factors also play a major role in these end points (not shown).

The utility of intermediate traits as end points. This greatly simplified schematic assumes there are 10 genes contributing equally to the clinical end point (ie, 10% each, faint dashed lines). Another level of complexity to the pathophysiology is superimposed by including 5 intermediate traits, each contributing 20% to the clinical outcome. In this example, genes 1 and 2 have a much larger effect on platelet reactivity (50%) than on the clinical end point (10%). Of course, environmental factors also play a major role in these end points (not shown).

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