 The development of GWAS and SNP heritability raises anew old philosophical questions regarding causal relationships. Researchers in the field are well aware of a handful of conceptual issues that provoke skepticism regarding the question of whether or not SNPs identified by GWAS are causal or not. John Dupré identifies GWAS as one among several approaches in the increasingly large effort to correlate genetic differences with phenotypic differences. He says that GWAS “uses the large amount of genetic data we now have about human populations to find correlations with medical outcomes—physiological and psychological disease” (2013, 285). Dupre goes on to say “as everyone involved in such research is aware, this is hardly a search for sufficient causes. GWAS will at best provide clues to the detailed causal processes involved in pathology” (2013, 286). Some GWAS researchers are more bullish on causation that Dupré indicates (See e.g. Plomin 2018). A well-known issue in population genetics, linkage disequilibrium, occurs when there is non-random association of alleles at different loci. GWAS researchers acknowledge that many of the SNPs of interest today are in linkage with many other SNPs in the genome. The implication is that it remains underdetermined whether SNPs are causal variants, or merely in linkage with causal variants (perhaps through evolutionary drift).