In addition, it is possible that impairment of Deaf1 action could account for increased levels of 5-HT1A autoreceptors in G/G subjects, and could also mediate a reduction in post-synaptic 5-HT1A receptors, suggesting Deaf1 as a potentially important mediator of transcriptional dys-regulation of the 5-HT1A receptor gene in depression. The gene discussed is HTR1A; the disease is depressive disorder.