Marsh et al. "Serotonin Transporter Genotype (5-HTTLPR) Predicts Utilitarian Moral Judgments"

It is very realistic. From the introduction.

Recent research demonstrates that participants' willingness to endorse utilitarian actions that require personally harming an innocent victim can be affected by variables that influence brain functioning, such as lesions of the ventromedial prefrontal cortex and pharmacological challenges [6], [7]. For example, respondents who receive a selective serotonin reuptake inhibitor (citalopram) are less likely to endorse utilitarian outcomes that result in harm to an innocent victim [7]. This may be because serotonin enhances the aversive emotional response to causing others harm, perhaps through its influence on brain structures like the amygdala, insula, and ventromedial prefrontal cortex, which are implicated in moral judgments and behavior [6], [8].

Endogenous serotonin neurotransmission is influenced by a functional 5′ promoter polymorphism of the serotonin transporter (5-HTT) in the human serotonin transporter gene SLC6A4, called 5-HTTLPR [9]. Relative to carriers of the long (L) form of the polymorphism, carriers of the short (S) form show reduced transcription, expression and function of 5-HTT, which influences the reuptake of serotonin from the synaptic cleft [10]. S-carriers are also more emotionally reactive to aversive stimuli than are L-carriers [11]. This difference may reflect S-carriers' increased activation in subcortical structures like the amygdala that are associated with negative affect and/or reduced prefrontal modulation of these structures by the prefrontal cortex [11].

This lab also has several previous studies dealing with both trolly-like problems and 5-HTTLPR.

I believe you. Suppose they were just looking for any genotype that might interact, and then there is a chance given all the zillions of genotypes that any genotype will show interaction just due to random chance.

If that's the case, that the interaction occurred by random chance, then you wouldn't expect the interaction to occur in a second experiment. But then -- is it really necessary to do two experiments? One could just look for interactions in the first half of the observations and then see if they are repeated in the second. Even so, you would still have a probability of some false positives but the probability would be smaller. So finally, I expect that any experimentalist working with such data would be aware of all of this and would look for a signal with a false positive probability of less than .05, so it would all be factored in the statistical analyses.

... so in the paper, is the probability of the interaction being significant calculated before or after considering there is some chance that any random genotype might show p<.05?

It's only a matter of time before some best-selling book claims that rational people are psychopaths.

Marsh's primary field is actually psychopathy research. You can see her lab's cv here a lot of the papers are there too, all PDFs though. A number of their paper's deal with the same genotype, the most obviously relevant one to your concern is a finding that s-carries experience fear-recognition impairment following tryptophan depletion. A google search for the 5-HTTLPR and psychopathy returns a mixed bag- it looks like the short allele might be a risk factor for ASPD which correlates with the psychopathy checklist. But it looks like there is a gene-environment interaction happening.

Depressingly, someone may have actually tested more directly for a correlation and it just got buried as a negative result.