After T. gondii infection, IFN-γ and other proinflammatory cytokines induce the activation of guanosine triphosphate cyclohydrolase-1 (GTP-CH1), which reduces the levels of phenylalanine (Phe, a precursor to norepinephrine) and tyrosine (Tyr, a precursor to dopamine), and may lead to a decrease in the levels of norepinephrine (NE) and DA in the synaptic cleft (Figure 2C), subsequently resulting in the onset of depression (Hsu et al., 2014; Kamal et al., 2022). This evidence concerns the gene IFNG and depressive symptom measurement.