The collective data are most consistent with the findings in other diseases, of strong effects being the exception but many risk loci of modest effects.
On the other hand, while GWAS have found many common variants that have modest effects on human common diseases, albeit some may have a key role, whereas the systematic identification of rare variants that are too rare to be detected in the GWAS and confer a substantial risk of the diseases is also required [36].
While the risk for hip fracture is partly heritable [174], the fact that many common genetic variants have modest effects on fracture risk [175] and that these are pleiotropic [176] is consistent with the data presented here.
While miRNAs may exert modest effects, yet on many targets, another possible answer to their significant effect on cell fate may lie in the level of the regulatory networks that miRNAs take central part in.
While some HIV-1 amino acid changes individually associate with decrease in VL, the compound image that emerges is one of a multiplicity of modest effects distributed across many residues.
It was concluded that there are probably many common variants in the human genome with modest effects on common disease risk.
The addition of GWAS to these established tools has the potential to widen the capability for quantification of effects on susceptibility of many individual genotypic variants that individually have relatively modest effects (Holloway et al. 2012).
In contrast, other perturbations such as Fsk and IBMX exhibit rather modest effects on the network despite affecting many other species in a qualitative sense.
Many GWAS are actually underpowered to detect these small or modest effects because of limited sample size [3].
Although GWAS have indeed identified certain susceptibility genes for many diseases, the genes thus far discovered mostly have been associated with small to modest effects [ 1- 5].
