Interestingly, we identified effector molecules of the AP-1 transcriptional program that particularly regulate the expression of neuronal remodeling and plasticity-inducing genes, many with known links to depression and antidepressant responses such as S100a10. Additionally, mice with a brain-specific deletion of c-Fos and c-Jun show defects in synaptic plasticity and axonal regeneration respectively [73, 74]. The gene discussed is JUN; the disease is depressive symptom measurement.