Therefore, this mechanism where NLRP3 inflammasome activation serves as the underlying basis between increased fatty acid levels, particularly LDL, being associated with higher CAD risk, is supported by our findings that CAD patients had increased LDL and inflammatory cytokines IL-1β, IL-6, TNF-α, and CRP, compared to non-CAD ones. The gene discussed is CRP; the disease is coronary artery disorder.