Background　As a subtype of T-type calcium channels， Cav3.2 is widely distributed in the spinal cord and dorsal root ganglia. Previous studies have shown that low voltage activation of T-type calcium channel may be involved in the pathogenesis of neural pathological pain. The role of Cav3.2 in chronic pain， especially pathogenesis of paclitaxel-induced pain hypersensitivity has increasingly become a research hotspot.　Objective　This review is to sum the mechanism of modulation of Cav3.2 in paclitaxel-induced hyperalgesia.　Content　The review includes the electrophysiological properties of Cav3.2， the feasible mechanisms involved in pain， and the relationship between different aspects of pain.　Trend　As a subtype of T-type calcium channels， Cav3.2 plays a critical role in the process of development of hyperalgesia. It is important for the treatment strategy of the chemotherapy-evoked neuropathic pain to clarify the physiological role of Cav3.2 and its role in the pathogenesis in paclitaxel-induced hyperalgesia.