Together, the above findings imply that while a TRPA1 antagonist, the effect of which is restricted to the periphery, delays the development of experimental diabetes-induced early anatomical and functional changes in TRPA1-expressing peripheral nociceptors, a peripherally restricted block of TRPA1 is expected to have a considerably weaker effect against diabetes-induced pain behavior than a TRPA1 antagonist that spreads also to the central nervous system (particularly to the spinal cord) to attenuate TRPA1-mediated amplification of nociceptive transmission in diabetes (Figure 1). This evidence concerns the gene TRPA1 and diabetes mellitus.