Research has indicated that certain hepatitis C patients develop major depression post-IFN-α treatment, potentially due to IFN-α can significantly down-regulate the expression of S100A10 protein in the hippocampus and cingulate gyrus of the brain, and the decrease of S100A10 protein leads to the decrease of the level of 5-hydroxytryptamine receptor 1b/4, which causes the impairment of synaptic 5-hydroxytryptamine signaling in the relevant neuronal nuclei, and ultimately leads to the development of depression in the organism (56). This evidence concerns the gene HTR1B and depressive symptom measurement.