But there is another layer of confusion, because WGS implies resequencing, and resequencing is only as good as your reference genome, and will distort results when the genome you're inferring is to far from the reference (reference bias).
The real mind bend will come when we have thousands or millions of whole genome de novo assemblies and we compare these to each other to do our GWAS. Only then are we going to have a hope of knowing what is actually causal in a genomic sense. Until then we remain in the land of association.
In nature, most adaptive variation appears to be large and structural. All the recent studies that have used whole genome assemblies to look at this have found the same thing. I would be surprised if this isn't the case for humans too. If it is, then much of current perspective on GWAS (both based on chips and WGS) will need to be rewritten.