First, high UA levels might trigger activation of the NLRP3 inflammasome analogously to what observed in gouty arthritis, where the uptake of monosodium urate crystals deposited in joints by macrophages leads to caspase-1–mediated maturation and release of IL-1β, IL-18, and downstream cytokines (IL-6, TNF-α, IL-33), sustaining and propagating systemic inflammation (Liu et al. 2015). The gene discussed is IL18; the disease is gout.