Taken together, the abovementioned studies of dysfunctional KCs suggest that oxidative stress-related signaling pathways make a difference in the pathogenesis of psoriasis, and it is worthy of decreasing cytokines gene expression and obstructing the autoimmune loop for the treatment of psoriasis effectively via quenching generation and traffic of triggers-induced pernicious ROS with ROS-depletion or -blockade approaches. The gene discussed is TBCE; the disease is psoriasis.