To explore this possibility, K5-IL-17C mice were genetically engineered to model increased epidermal IL-17C expression [13], and develop a spontaneous skin phenotype similar to human psoriasis that includes the development of disease after birth (i.e. the phenotype begins to appear at ~6–8 weeks of age), well-demarcated skin lesions with clear gross demarcation between uninvolved and involved skin, an IL-12/23-Th1/Th17 immune cell phenotype, and improvement of skin pathology upon treatment with TNF-α antagonists [13]. Here, IL17C is linked to psoriasis.