Posttraumatic stress disorder (PTSD) severely deteriorates the quality of life of an increasing number of people. Fortunately, the majority of trauma-exposed individuals recovers successfully and shows resilience to these negative consequences of trauma. Understanding the neural underpinnings of trauma resilience versus susceptibility might be key to improve PTSD prevention and treatment. Maladaptive, intrusive trauma memories are a core symptom of PTSD. These memories are characterized by poor contextualization, suggesting impaired hippocampal recruitment in the trauma memory trace. This may be caused by epigenetic dysregulation. Histone acetylation is a particularly promising candidate, as it is a major epigenetic regulator of memory and is modulated by stress exposure. To investigate this, we used ArcTRAPxtdTomato transgenic mice, in which trauma memory engram neurons were fluorescently labelled for targeted analysis. Animals were subjected to a stress-enhanced fear-learning protocol that induced PTSD-like symptoms in a subset of mice, while other mice appeared resilient. After re-exposure to the trauma context, the animals were euthanized and activated hippocampal neurons during trauma memory encoding (labeled by tdTomato) and remote recall (by c-fos immunohistochemistry) were analyzed. Furthermore, the levels of a relevant histone acetylation mark, H3K9ac, were assessed in these engram and non-engram cells and compared between susceptible and resilient mice. The first results indeed indicated a differential distribution pattern of trauma memory engram neurons between resilient and susceptible mice. These were promising first steps in the pathway of uncovering how neuro-epigenetic mechanisms mediate interindividual differences in stress resilience.