Recently, Yang et al.43 showed (i) that 45% of the phenotypic variance (roughly half of the heritability) of human height can be explained by considering all single-nucleotide polymorphism SNPs simultaneously in a linear model analysis, implying that most of the heritability is not missing but is as yet undetected due to effect sizes of individual variants being too small to reach significance in GWAS conducted to date; and (ii) that the remaining heritability can be ascribed to incomplete linkage disequilibrium (LD) between causal variants and genotyped SNPs. Insufficient LD is likely to occur if causal variants have lower minor allele frequency (MAF) than the genotyped SNPs.44
