The administration of pro-inflammatory cytokines (e.g., INF-α) or endotoxin have been shown to reduce neural responses to reward [67, 68], while the relationship between plasma high-sensitivity CRP (hs-CRP) and the brain reward circuit has been investigated in depression, at the level of resting-state functional connectivity [21, 65]. The gene discussed is IFNA17; the disease is depressive disorder.