Cyclothymia is a chronic mood disorder characterized by alternating subclinical hypomanic and depressive symptoms. Despite its classification within the bipolar spectrum, it remains underdiagnosed and understudied, particularly regarding its biological basis. Research suggests that alterations in stress-related systems, particularly involving the hypothalamic-pituitary-adrenal (HPA) axis may contribute to symptom development. This paper explores the potential role of NR3C1 gene methylation, known to influence glucocorticoid receptor expression, in shaping mood instability linked to early-life adversity. Using the Network-Oriented Modelling (NOM) approach, a multilevel adaptive network model was developed to explore two simulation scenarios: one modeling lasting NR3C1 methylation changes due to early-life adversity, and another introducing a hypothetical epigenetic therapy aimed at countering these effects. The simulations suggest that such methylation-related changes could influence cortisol regulation and, in turn, contribute to long-term emotional fluctuations. When the therapeutic intervention was introduced, the model indicated a potential shift toward rebalancing this disrupted system. While these findings are speculative and based on theoretical modeling, they provide a perspective on how epigenetic and environmental influences might interact in the development of cyclothymic symptoms. Overall, the work highlights the need for continued research into the biological foundations of mood disorders and possibilities for innovative treatment approaches.