While the inhibition or knockout of TRPA1 reduces nociceptive responses to electrophilic irritants, oxidative stress, and inflammatory pain models (Bautista et al., 2006; Kwan et al., 2006; Dai et al., 2007; McNamara et al., 2007; Eid et al., 2008), a role for TRPA1 has also been reported for other physiological and pathophysiological processes such as endothelium-dependent cerebral artery dilation (Earley et al., 2009), anxiety (de Moura et al., 2014), cognition and memory (Lee et al., 2016a,b), which are unlikely to be mediated by sensory nerves. This evidence concerns the gene TRPA1 and Anxiety.