PD-1 inhibitors exert their effects by blocking PD-1/PD-L1 interactions, thereby reversing T cell suppression and resulting in hyperactivation of psoriasis-associated Th1/Th17 subsets accompanied by dysregulated cytokine production (27).These activated T cells secrete various cytokines including interferon-γ, IL-1, IL-17, and IL-22 (28),which subsequently migrate to cutaneous tissues and activate resident immune cells (keratinocytes, dendritic cells, and neutrophils), ultimately inducing or aggravating psoriatic lesions (29). The gene discussed is IL17A; the disease is psoriasis.