Accumulating studies have found that some possible mechanisms were involved in the development of IFN-α-induced depression, including dysregulation of monoaminergic and glutamatergic neurotransmitter systems (Capuron et al., 2003; Haroon et al., 2014), alterations of activities of the HPA axis (Felger et al., 2016), and impairment of neuronal survival and plasticity (Hoyo-Becerra et al., 2014; Zheng et al., 2015). This evidence concerns the gene IFNA1 and depressive symptom measurement.