Zhang and colleagues found that STAT1-induced miR-17-92 cluster promoted keratinocyte proliferation by suppressing cyclin-dependent kinase inhibitor 2B (CDKN2B) and increased the chemokine production via inhibition of suppressor of cytokine signaling 1 (SOCS1), suggesting miR-17-92 as a potential therapeutic target for psoriasis [103]. This evidence concerns the gene SOCS1 and psoriasis.