Similar to tofacitinib, these two peptido-mimetics were able to switch off the IFN-γ- and IL-22-dependent inflammatory/immune responses of keratinocytes in cutaneous disease contexts characterized by the presence of IFN-γ-releasing Th1 and IL-22-releasing Th22 infiltrate, such as psoriasis and squamous skin cell carcinoma, respectively [15, 16]. The gene discussed is IL22; the disease is psoriasis.