In terms of mechanism, previous studies have shown that in psoriasis, NLRP3 may recognize microbial components (e.g., lipopolysaccharides) or endogenous danger signals (e.g., urate crystals, reactive oxygen species), activate caspase-1, and cleave GSDMD, leading to pyroptosis and IL-1β release, thereby amplifying skin inflammation [6,27]. The gene discussed is IL1B; the disease is psoriasis.