ABSTRACT
Interactions between different genes, coined the epistasis, have long been recognized to play a central role in shaping the genetic architecture of a quantitative trait (Whitlock et al., 1995; Wolf, 2000; Cheverud, 2006). Recent genetic studies from vast quantities of molecular data have also indicated that epistasis is of paramount importance in the pathogenesis of most common human diseases, such as cancer or cardiovascular disease (Cordell, 2002; Moore, 2003; Talkowski et al., 2008), and patients’ responsiveness to a medicine (Lin et al., 2007). The evidence for this is the nonlinear relationship detected between genotype and phenotype. The decipherment of interconnected networks of genes and their associations with disease susceptibility has become a pressing demand for a detailed understanding of the genetic basis for disease processes (Moore et al., 2008).
