I also work in this field. This article is interesting and gets some things right (although is overly alarmist, in my opinion). There are opinions in this artic

I also work in this field. This article is interesting and gets some things right (although is overly alarmist, in my opinion). There are opinions in this article that I disagree with, however. For example, I disagree with the statement that "... classical Mendelian genetics based on family studies has identified far more disease-risk genes with larger effects than GWAS research has so far." First, under selection, one would not expect common variants to have tremendous, deleterious effects in general. Second, it is not true that Mendelian studies are superior to GWAS in, say, lipoprotein genetics. There, virtually all of the genes known from studies of Mendelian disorders have been re-discovered through GWAS, with many new findings that were previously unknown. Furthermore, a substantial portion of lipid heritability (~20%) could be explained by GWAS-identified loci as of January 2009. There there is little reason to believe that common variants (>=5% minor allele frequency) should explain all of heritability; so far, so good. The upcoming 100,000 individual lipids GWAS should do a pretty good job of sucking at the marrow for the remaining common variants. We work with the tools that we have. SNP-chips enabled GWAS. Now that "next-gen" sequencing (worst buzzword ever) has brought down costs, the thousand genomes project will provide us with a list of nearly all variants with MAF>1%. Well-funded groups can afford to deep sequence their population of choice. These provide information that is complementary to the information obtained by GWAS. In conclusion, GWAS is good for finding common variants. Imputation from thousand genomes should be good for finding low-frequency (>1% MAF) variants. And sequencing is good for finding rare variants. There is no crisis.