Well, Khader, you should have been at ASHG last week - and should have then run from talk to talk where all kinds of folks presented very similar situations. The MYC paper GWW cites is an example that comes to mind as well. In fact, I saw talks by two of those authors. I also saw a presentation of using ENCODE data to annotate the GWAS hits - so I agree with Sean's excellent idea. My notes from these talks are on my blog: Wasserman, Degner's use of ENCODE data, and Stamatoyannopoulos' talk on using ENCODE.
This is just a start, though. There is certainly a lot of ideas on this topic. Generally, the SNPs in gene deserts are SNPs regulating either expression of a distant protein-coding gene or are in/near to a non-protein-coding (RNA) gene. Ideally, you would have expression data (either from a genome-wide chip of mRNA probes) or RT-PCR data across the region (in which you can identify those novel transcription products) to compare to the GWAS data to look for a type of eQTL.
Added on 12 Jul 2011: The continued evolution of the epigenomebrowser.org site makes it a very good place to go to get the data mentioned here. There are now some very nice displays of Stamatoyannopoulos' DNaseI hypersensitivity sites, tissue-specific histone methylation and acetylation marks as well as transcription factor ChIP data.
When you say causal along with non-genic, it is not clear. Is there a specific functional motif that is changed by the SNP or is it associative in phenotype?
I mean SNP is in a region of a genome where no known gene is annotated. Gene desert / non-genic region are generally used for such regions for example: http://genome.cshlp.org/content/20/9/1191.full http://genome.cshlp.org/content/15/1/137.full
I feel it is better to call the SNP associative than causal. Causal seems more definitive reg: fxn
I called it as causal, because of it's significant p-value and OR.
So correlation == causation these days?
@Vijai / Adrian: Question edited.
@Vijai / Adrian / Aaron : Question edited.