 Since Maher (2008) first coined the term “missing heritability,” statisticians and geneticists have written extensively about the issue. In nearly all cases, contributors speak to possible explanations for why there is missing heritability and emphasize technological and methodological solutions that should close the numerical gap between traditional and SNP heritability estimates. Explanations for missing heritability typically focus on various manners in which standard format GWAS are unable to track genetic effects that are unavoidably part and parcel of twin and family studies. Notably, contributors appeal to non-linear interactions between genetic variants (‘GxG interaction’, or epistasis). Epistatic interactions between SNPs entail that the effect of a given SNP will be modified (enhanced or diminished, for example) in the presence of another SNP, which violates the additivity assumption of SNP heritability. Similarly, gene-environment interaction and epigenesis have been proposed as explanations for missing heritability (Zuk et al. 2012). Specific variants or groups of variants may have effects that are enhanced, diminished, or even muted with different environments, again violating the additivity assumption of SNP heritability. Some missing heritability may be attributable to the presenence of low-frequency, high-penetrance variants, which require massive samples to detect (Zuk et al. 2014). (See Eric Turkheimer (2011, 2012) and Matthews &amp; Turkheimer (forthcoming) for a more thorough review of explanations of and solutions to missing heritability.)