Although the numbers of PV-INs and somatostatin-positive inhibitory interneurons were observed at significantly low levels in a chronic inflammatory pain model of ACC [13], activation of PV-INs but not somatostatin-positive interneurons using optogenetic or chemogenetic techniques to compensate for the diminished inhibitory activity reduces peripheral mechanical hypersensitivity and alleviates pain-anxiety-like behaviors [13,14], indicating the important role that PV-INs play in pain modulation. The gene discussed is SST; the disease is Anxiety.