This shortfall in explained genetic variance, popularly referred to as “missing heritability” (Maher 2008; Manolio et al. 2009), has been widely observed for other complex disease phenotypes, leading many to re-evaluate the validity of the common disease-common variant hypothesis and suggest a more central role for rare variants, epigenetics and/or genetic interactions in pathogenesis. New analytical approaches, however, have begun to bridge the heritability gap, indicating that much of the additive genetic variance of complex traits, such as human height (Yang et al. 2010), intelligence (Davies et al. 2011) and schizophrenia (Lee et al. 2012), are arguably captured by common GWAS markers.
