I've said many times in the past that people who think they can say something deeply significant about the nature of phenotypical variation between "races" based only on the identification of a single allele of uncertain effect are at best fools and at worst liars, and this PLoS paper drives home the point I was making in a straightforward way; following is the synopsis.
Most of the differences in phenotype between unrelated members of a species are polygenic in nature. Because of their ubiquity and importance, these polygenic (or quantitative) traits have been intensively studied, and a variety of techniques have been proposed to identify and characterize quantitative trait genes (QTGs). Indeed, the main application of the recently published human HapMap project is to identify the genes responsible for diseases that are quantitative in nature. Using a well-defined Saccharomyces cerevisiae quantitative trait locus containing three QTGs (MKT1, END3, and RHO2), the authors used deletions to analyze the contributions of each gene to phenotype, singly and in combination, and found a variety of interactions. Expression analysis showed no difference in steady-state mRNA levels between alleles of the three genes. Homologous allele replacement identified the phenotypically relevant differences between alleles of each gene, which were single coding polymorphisms for two genes (MKT1 and END3) and the 3′ untranslated region of one gene (RHO2). Finally, analysis of multiple genetic backgrounds showed that the phenotypes conferred by these genetic variants were not conserved. The results show that the techniques proposed to identify QTGs, such as expression analysis and marker-trait association, have profound limitations, and that unbiased genome-wide approaches are needed to dissect quantitative traits. The results also demonstrate the complexity of the genetic interactions that affect quantitative traits and the value of the S. cerevisiae system in studying these traits.Anyone who expects things to be easier with humans than they are with short-lived organisms for which no restrictions on experimentation exist is living in a dream world. It will likely take several decades to unravel the genetic basis for variation in such amorphous traits as "IQ" or personality, assuming it ever becomes possible at all, and anyone who claims otherwise is a charlatan selling snake oil.
PS: This abstract from a paper on common human diseases also presses home the same point - as much as population geneticists might wish it were otherwise, the evidence seems to indicate that epistasis is in fact a ubiquitous phenomenon, while complex interactions which defy simple "additive gene" expectations are almost certainly the rule rather than the exception. In plain English, don't expect any findings that some putative "IQ boosting alleles" can be found in some populations and not others to tell you anything whatsoever about their respective "innate" intellectual abilities; don't even assume that the existence of a single allele in multiple populations means that its effects need be the same in all of them.