IL-12 induces the differentiation of naïve cells into Th1 cells, secreting TNF-α and IFN-γ.[29,30] These cytokines result in the proliferation of keratinocytes, upregulation of endothelial adhesion molecules and angiogenic mediators, as well as elevated immune cell infiltrates, further worsening the psoriasis progression.[30] Therefore, SII based on neutrophils, platelets, and lymphocytes might increase psoriasis risk via the involvement of immune cell response. The gene discussed is TNF; the disease is psoriasis.