The findings of the present study suggest that the molecular mechanism behind (long-term) colitis protection by CPZ is the sustained (over)stimulation and consecutive desensitization of TRPA1 and TRPA1/TRPV1 co-expressing neurons rather than antagonism to TRPV1, since TRPV1-deficient mice were as well-protected by CPZ enemas as were WT mice. This evidence concerns the gene TRPA1 and colitis.