Taking together the evidence in AN of elevated pro-inflammatory cytokines [2,3], reduced concentrations of BDNF and VEGF-A [76], and reduced hippocampal volumes [77,78], a key area for adult neurogenesis, it could be hypothesised that this mechanism may be at play in AN, as proposed in the depression literature [34,79]. The gene discussed is BDNF; the disease is depressive symptom measurement.