The pathophysiology of SLE involves dysregulation in both innate and adaptive immune responses, characterized by impaired apoptotic cell clearance and dysfunctions in B- and T-cell activity [4]. In the contrary, psoriasis is a chronic auto immune inflammatory skin disease that is predominantly a T-cell-mediated disorder driven by the IL-23/Th17/IL-17 pathway. This pathway plays a central role in driving a self-sustaining inflammatory cascade, leading to dysregulated keratinocyte proliferation and differentiation, which contributes to the development of characteristic psoriatic lesions. The gene discussed is IL17A; the disease is psoriasis.