If G9a/GLP have both shown to play a role in the methylation of lysine 9 of histone 3, then the "postnatal knockout" of G9a reducing the anxiety phenotype in mice could lead us to do more research in how H3K9 methylation regulates expression of genes involved in anxiety.

Corticosterone in rodents is equivalent to cortisol in humans, the primary glucocorticoid released in response to stress. If decreased levels of acetylation on Lysine 9 of Histone 3 is observed in rodents with higher levels of corticosterone, this suggests that chromatin at H3K9 becomes more condensed, leading to reduced transcription of stress-regulating genes

If an elevated level of H3K9me3 associated with the GR promoter is detected in the amygdala and hippocampus of low anxiety rats, it suggests that the gene regulated by the GR promoter produces a protein that is linked with anxiety. Because trimethylation of a promoter site almost always reduces transcription, we will observe less of that gene. In this case, higher methylation levels of the promoter is linked with lower anxiety, which means that the promoter produces anxiety promoting proteins

H3K9ac increases as a result of TSA because it prevents the deactylation of H3K9, this likely is tied directly to GR expression because preventing deacetylation will upregulate the expression. . Concurrently, the TSA decreases CRF mRNA levels, thereby reducing pro-anxiety signaling. Overall, these findings show how HDAC inhibition can modulate histone acetylation to regulate stress-related gene expression and help stop anxiety-like behaviors

Because early stress decreased dimethylation of Lysine 9 on Histone 3 for 2 months we can identify this as an example of epigenetic change. The findings show how histone modifications such as dimethylation at promoter regions can regulate gene expression as a result of environmental/external factors.

An increase in H3K9me2 means that there will be less transcription of BDNF. Seeing decreased Bdnf, which is essential for synaptic plasticity and emotional regulation. Since high levels of BDNF have been linked to both improved learning and heightened anxiety behaviors, this relationship suggests that the levels of H3K9me2 play a massive role in balancing cognitive and emotional outcomes, which falls in line with our topic of anxiety.

If a protein that supports neuron growth and learning also promotes the development of the anxiety phenotype when up-regulated during transcription, then regulated neural plasticity pathways could also influence the development of anxiety.

Hyperacetylation of histones will increase transcription, which naturally will lead to an increase in the BDNF exon IV mRNA. This means the protein coded for by the BDNF exon during translation plays a role in repressing learned fear response. This could imply a relation between this exon and anxiety because anxiety is partly a learned fear response.