In experimental disease models, mice with imiquimod-induced psoriasis-like dermatitis, which were treated with an anti-IL-12/IL-23p40 monoclonal antibody (p40 mAb) showed reduced epidermal thickness and increased transepidermal water loss, as well as suppression of IL-23p19, IL-17A, IL-22 and keratin 16 gene expression, suggesting that p40 mAb not only improves dermatitis symptoms, but is also effective against skin barrier dysfunction in those mice (Takahashi et al., 2018[178]). The gene discussed is IL17A; the disease is psoriasis.