TRPV1 is a non-selective cation channel that is mostly located on central and primary afferent sensory neurons. TRPV1 is activated by noxious painful stimuli such as acid (low pH), noxious heat (>430C), voltage, components of the inflammatory, oxidative stress and vanilloids. TRPV1 has important role on detection and transmission of painful stimuli. In this review article, the authors summarize the recent information of pain literature to understand the etiology of the pain. The effects of TRPV1 on different types of neuronal pain are investigated in the laboratory and clinical trials. TRPV1 is reported to contribute to acute, chronic pain, such as osteoarthritis, neuropathic pain, migraine, bone cancer pain. It is also reported that TRPV1 takes part in pain processing and modulation, thermoregulation, osmoregulation among other functions. Activation of TRPV1 has important role on persistent cough, chronic obstructive pulmonary disease, bladder hyperactivity associated with bladder inflammation in human. TRPV1 is regulated / activated by some lipids such as phosphatidylinositolbiphosphate (PIP2) and lysophosphatidylcholine (LPA). Hence, PIP2 and LPA have been described as modulator and allosteric activator of the channel. A range of inflammatory mediators and growth or tumor factors are known to contribute to hyperalgesia via sensitization of TRPV1 through activation of kinase pathways that can lead to direct receptor phosphorylation at multiple intracellular sites. In conclusion, immunohistochemical, biophysical, pharmacological characterization of these channels might provide the intellectual and technical infrastructure for developing new classes of analgesic drugs.