Additionally, it suggests a direct stimulatory effect of reactive oxygen species (ROS) on nociceptor firing via transient receptor potential ankyrin subtype 1 (TRPA1) ion channels and an indirect role for ROS in sensitizing sensory afferents via the release of a major migraine mediator calcitonin gene-related peptide (CGRP) from nociceptor neurons [43]. The gene discussed is TRPA1; the disease is migraine disorder.