Though TRPA1 proved not to be a key regulator of TcR (anti-CD3 only) stimulated calcium signaling in our studies, its function negatively modulated a sustained elevation of intracellular calcium level of CD8+ T lymphocytes triggered by imiquimod, the most frequently used in vivo psoriasis-inducing agent in model systems [87]. The gene discussed is CD8A; the disease is psoriasis.