In a murine model of interleukin-23 (IL-23) dependent psoriasiform dermatitis, two novel dimeric CCL20 variants induced (i) intracellular calcium release, (ii) minimized chemotactic activity, (iii) inhibited CCR6-mediated T cell migration, (iv) up-regulation of interleukin-17 (IL-17) and interleukin-22 (IL-22), and (v) the prevention of psoriatic inflammation, thus highlighting the role of CCR6 as a controllable therapeutic target [19]. The gene discussed is IL22; the disease is Psoriasiform dermatitis.