That's quite the sweeping claim. Some quick googling suggests otherwise.

"Chronic stress induces significant gene expression changes in the prefrontal cortex alongside alterations in adult hippocampal neurogenesis"

>In this study, unpredictable chronic mild stress in mice resulted in a deficit in neuronal dendritic tree development and neuroblast migration in the hippocampal neurogenic niche. To investigate molecular pathways underlying neurogenesis alteration, genome-wide gene expression changes were assessed in the prefrontal cortex, hippocampus and the hypothalamus alongside neurogenesis changes. Cluster analysis showed that the transcriptomic signature of chronic stress is much more prominent in the prefrontal cortex compared to the hippocampus and the hypothalamus. Pathway analyses suggested huntingtin, leptin, myelin regulatory factor, methyl-CpG binding protein and brain-derived neurotrophic factor as the top predicted upstream regulators of transcriptomic changes in the prefrontal cortex. Involvement of the satiety regulating pathways (leptin) was corroborated by behavioural data showing increased food reward motivation in stressed mice. Behavioural and gene expression data also suggested circadian rhythm disruption and activation of circadian clock genes such as Period 2.

[1] https://academic.oup.com/braincomms/article/2/2/fcaa153/5912...

You didn't read the paper, and you didn't understand it. It didn't make a link between gene expression and behavioral changes. It just noted a change in gene expression in a handful of mice, basically the same study as the above.

>Many target genes, upstream regulators and signalling pathways involved in the PFC response in our study could be linked to dendritic remodelling and spine atrophy, a well-described effect of chronic stress on the PFC. Based on the IPA pathway and upstream regulator analysis, glutamatergic and calcium signalling, as well as Htt and Bdnf-centred networks stood out as the most significantly involved. Indeed, repeated stress is known to cause suppressed glutamate receptor expression and signalling in the PFC, which is thought to be linked to dendritic atrophy (Yuen et al., 2012). Many recent studies have explored the antidepressant potential of ketamine in chronic stress animal models of depression, strengthening the glutamatergic theory of depression (Zhu et al., 2015; Sun, 2016). In addition, disruption of glutamatergic signalling has been previously linked to hyperactivity (Procaccini et al., 2011).

The animals in the study, as expected, showed depression-associated and hyperactivity behaviors. This study wasn't looking at any specific thing in a fine-grained sense, let alone trying to establish causation. But "no link" seems like quite a stretch.

Yes, of course they showed effects from the UCMS. But not one single sentence in that report said that those effects were from gene expression. YOU are the only one adding a link there. It's easy for someone like you to just say there's a link, but not even the study pretends to say there's a link between the results of trauma are because of gene expression.