Specifically, we hypothesize that: (1) disrupted IL-6 secretion (i.e., increased total output or diminished diurnal rhythm) is associated with perturbed (i.e., increased or decreased) amygdala activity in response to emotional stimuli; (2) disrupted IL-6 secretion is correlated with greater depressive/anxiety symptoms; and (3) disrupted IL-6 secretion can be predicted by the interactions between psychosocial stressors and IL6 or IL6R SNPs. The gene discussed is IL6R; the disease is Anxiety.