Specifically, the role of IL-17-mediated activation of the NLRP3 inflammasome complex in psoriasis inflammation is widely demonstrated,[14,15] meanwhile, the activation of NLRP3 inflammasome complex is also closely related to cell death like pyroptosis, apoptosis and necrosis, which ultimately leads to elevated production of IL-1β and IL-17.[16] Triggers like infection can also activate IL-23/IL-17-mediated immune responses by inducing caspase-mediated apoptosis of KC.[17] Necrosis could promote IL-17 expression and contribute to psoriasis as well. The gene discussed is CALCA; the disease is psoriasis.