Moreover, our data clearly indicate that TRPV1 is not only a sensor of pain and temperature variations that initiate the propagation of a signal among neuronal cells, but it may also act on neuronal as well as non-neuronal cells as a molecular sensor of temperature variation and of other non-thermal cellular stresses, such as inflammatory stimuli (sepsis), activating HSP expression. This evidence concerns the gene HSP90B2P and Sepsis.