During development of skin inflammatory diseases, keratinocytes, the predominant cell type in the epidermis, express both SOCS1 and SOCS3 molecules in response to a plethora of IFNs and ILs, mostly derived from T lymphocytes, which inhibit in a negative feedback loop the JAK/STAT pathways activated by these inducing stimuli (82). This evidence concerns the gene SOCS3 and inflammatory skin disease.