Although new neuron production was responsive to IFN-α and minocycline, the density of NeuN+ mature neurons in the granule cell layer in the DG was not affected by these treatments, similar to those in the CA3, amygdala, prefrontal cortex, and cingulate cortex, non-neurogenic areas implicated in the pathology of depression (Hulvershorn et al., 2011; Belzung et al., 2014; Supplementary Figure 1B). The gene discussed is IFNA1; the disease is major depressive disorder.