This suggestion rests on both the cytokine model of depression (47, 48) and on the the cytokine model of cognitive function that outline the role of cytokines (e.g., TNF-α, IL-6, and IL-1β) in regulating sickness behavior and neurobiological processes subserving cognition, i.e., synaptic plasticity, synaptic scaling, neurogenesis, neurotransmission, and long-term potentiation/depression (LTP/LTD) that are relevant to cognitive function in depression (49). This evidence concerns the gene IL1B and depressive disorder.