In particular, the complement component 3 has been shown to mediate systemic IFN-β-induced changes in neuroinflammation and behavior of mice subjected to unpredictable chronic mild stress and a similar correlation has also been shown in humans, as increased expression levels of IFN-I stimulated genes and significant correlations with complement 3 and inflammatory markers have been observed in the prefrontal cortex of individuals with depression who died by suicide [49]. The gene discussed is C3; the disease is depressive symptom measurement.