Valid arguments are found for both theories: while deletion of the epidermal proteins JunB/activator protein1, IKK2 or STAT3 overexpression are each sufficient to induce a psoriasis-like phenotype in mice [3]–[5], the description of patients with both psoriasis and eczema or ACD in parallel argues for specific local stimuli inducing either psoriasis or eczema [6]. Here, STAT3 is linked to psoriasis.