Hi, everyone
Some questions about the GxE model:
From Wikipedia,
The basic ACE model relies on several assumptions, including the absence of assortative mating,[4] that there is no genetic dominance or epistasis,[5] that all genetic effects are additive, and the absence of gene-environment interactions.[3] In order to address these limitations, several variants of the ACE model have been developed, including an ACE-β model, which emphasizes the identification of causal effects,[3] and the ACDE model, which accounts for the presence of dominant genetic effects.[6]
So why is the GxE model still valid?
Another question: Because rGE can result in spurious detection of G E, it is advisable to incorporate SES into the moderation model as a fixed regressor, which will partial out any phenotypic variance due to correlation between SES and A (Purcell, 2002; van der Sluis, Posthuma, & Dolan, 2012).
I just can’t understand how the rGE is out in GxE model?