And/or (iii) the blockade of this receptor does not only inhibit the function of IL-36 ligands but also of their antagonist; a psoriasis study by Blumberg and coworkers proposed a mechanism by which the overproduction of the ligand IL-36α together with the lack of signaling inhibition by the antagonist IL-36Ra shifts the balance between these cytokines and thereby induces the phenotype [3]. Here, IL36A is linked to psoriasis.