The inhibition of KV1.3 with PAP-1 reduced hyperalgesia, M1 polarization, and the expression of NLRP3, caspase-1, and IL-1β, suggesting that KV1.3 channels may play a key role in neuropathic pain by promoting M1 microglial polarization and activating the NLRP3 inflammasome [275]. The gene discussed is KCNA3; the disease is neuropathic pain.