As noted by Yang et al. (34), heritability estimates obtained via the use of GWAS SNPs are likely underestimates of the true heritability due to common variation because of incomplete LD between causal variants and available SNPs and the fact that causal variants may have lower MAF when compared with all other SNPs examined.
In fact, over 90% of sequence variation among individuals is due to common variant sites, most of which arose from single historical mutation events on the ancestral chromosome [5].
This means that between and within the age groups, differences between observed thresholds and observed variances across age and sex appear to be due to common factor variation and real differences in the TP-construct/factor mean.
These estimations are based on the genetic covariance between untransformed peer problem measures at different ages, which is due to common measured genetic variation.
A graphical display referred to as a control chart provides a basis for deciding whether the variation in the output of a process is due to common causes (randomly occurring variations) or to out-of-the-ordinary assignable causes.
When we used phylogenetic models that control for similarity between species, due to common descent, and focused on variations within a single lineage (DRB1*03), the positive relationship between different substitution rates and allelic polymorphisms was still robust.
In Model 8 (Table 4), the variance of the Intercept factor was decomposed into additive genetic influences (A), variation due to common environmental effects (C) and unique environmental influences (E).
This suggests that variation in HbA1c levels due to common, nonglycemic effect variants might influence only minimally diagnosis or misclassification of diabetes.
We found that for most of the perturbations, variation in lethality penetrance is due to common alleles at many contributing cryptic loci.
GWAS rely on the common disease-common variant model, stating that most of the genetic variation in common complex diseases is due to common variants [20, 21].
