Of course it could turn out that both genes, rather than being related to the A or N loci, are just "modifier genes" having to do with impulsivity or modulation of aggression.
I suspect that someone adept in interrogating the ALFRED database could come up with some other candidate genes for the N locus in short order by comparing allelic frequencies of genes in sanguine and non-sanguine geographic locations.
We were attracted to the study for several reasons:
1. Finland (sanguine/Introspective habitancy) is adjacent to a large non-sanguine area (northwetern Russia), so one might expect that very violent offenders would have a preponderance of non-sanguine A types.
2. The case-control study illustrates how one could use the principle of entanglement to locate the N locus when part of the population is non-sanguine. The study measures phenotypes of aggression (A trait), but we are using it to sort out the N locus on the assumption that extreme A trait is non-sanguine. The entanglement principle is that the absence of trait N necessarily implies the presence of trait A, so there can be no overlap between non-sanguinity and the absence of aggression.
By this reasoning, if one assumes that violent antisocial behavior is positively associated with non-sanguine A types (in relatively polymorphic habitancies), then to find the N genetic locus one should look for genes that are related to antisocial behavior.
3. The study raises the question that two genes could be responsible for non-sanguinity, rather than a single N locus. This is possible in the NPA model. However, not more than two (not closely linked) genes, as otherwise the transmission of non-sanguinity from a parent to a child would be an unusual event, which we know is not the case. (It would be unusual because the probability of transferring an intact array of many unrelated genes from a parent to a child would be very low).
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