The involvement of PAR-4 in the sensitization of TRPA1 is poorly studied, but a recent finding demonstrated its potential role in pruritus: the dorsal intradermal administration of the PAR-4 agonist peptide AYPGKF-NH2 elicited intense scratching behavior via a SP release in mice, which was abolished by the TRPV1 and TRPA1 antagonists SB366791 and HC-030031, respectively (Patricio et al., 2015), but not in TRPA1-deficient mice. Here, TRPA1 is linked to Pruritus.