Anxiety disorders (ADs) are highly prevalent, heterogeneous group of psychiatric conditions with an impressive public health impact. Twin and family studies confirm a moderate heritability (typically 30-50%), suggesting a clear genetic predisposition. However, the complexity and polygenic nature of ADs, where many common genetic variants each contribute only a small effect, have meant that Genome-Wide Association Studies (GWAS) have had limited success in identifying major causative loci. This gap underscores the critical role of environmental factors and their interaction with the genome in disease pathogenesis. Epigenetics provides the critical mechanism for this gene-environment interaction. These reversible modifications, which include DNA methylation, histone modifications, and non-coding RNAs (ncRNAs), alter gene expression without changing the underlying DNA sequence.  The majority of environmental stressors, particularly early-life adversity, can lead to persistent epigenetic changes, biologically embedding vulnerability and altering an individual's response to stress later in life.The aim of our study was to investigate the role of genetic polymorphisms, genetic variants and epigenetic modifications in anxiety disordersWe have done literature review and summarised the dataResearch, mainly utilizing animal models, has identified epigenetic modifications in brain regions critical for stress and emotion regulation, such as the amygdala, hippocampus, and prefrontal cortex (PFC). These modifications often target genes involved in the Hypothalamic-Pituitary-Adrenal (HPA) axis (e.g., NR3C1, FKBP5) and neurotransmitter systems (e.g., GABAergic and serotonergic pathways). For instance, altered DNA methylation of the NR3C1 gene, which encodes the glucocorticoid receptor, has been implicated in an abnormal stress response.DNA methylation is a crucial epigenetic mechanism that plays a significant role in the pathophysiology of anxiety disorders by influencing gene expression in brain regions associated with stress and emotion.In conclusion, the current understanding of Anxiety disordres demonstraits a complex interplay between an individual’s genetic predisposition and epigenetic alterations induced by environmental exposure. Future research integrating large-scale genetic and epigenetic data across diverse populations is essential to fully characterize the risk architecture of ADs. This neuroepigenetic perspective offers promising avenues for identifying novel biomarkers for risk prediction and developing targeted, epigenetic-based therapeutics to modulate maladaptive gene expression patterns.