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.

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 the lysine 9 of histone 3 contains a nucleotide strand that codes for a gene that influences 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.