We further characterized the InflammaSkin® model for its capacity to establish an interplay between activated Th17 cells and keratinocytes, as exemplified by the increased expression of the epidermal markers, Keratin‐16 and S100A7, known to be highly upregulated in psoriasis lesions.[19] Importantly, we provide evidence that the psoriasis‐like inflammatory interplay between Th17 cells and keratinocytes can be inhibited by topical treatment with two classes of drugs of therapeutic relevance for psoriasis, a corticosteroid and a PDE4 inhibitor. Here, S100A7 is linked to psoriasis.