The results of this costly international exercise have been disappointing. About 2,000 sites on the human genome have been statistically linked with various diseases, but in many cases the sites are not inside working genes, suggesting there may be some conceptual flaw in the statistics.
Erm… or maybe many common variants affecting the risk of complex diseases simply aren’t found in protein-coding regions? That’s the (biologically entirely plausible) hypothesis that most complex disease geneticists are working under right now.
I’m guessing the statement is an oblique reference to the recent synthetic association paper
from David Goldstein’s group? If so, it’s worth noting that the claims made in that paper are seriously
contentious among others in the field.