Targeting individual interleukins (IL) in patients with atherothrombotic residual risk despite evidence-based standard therapy, has achieved a lower effect than expected (e.g., only a 15% risk reduction of adverse events in patients treated with canakinumab, an IL-1β blocker) suggesting that other products of the inflammasome might be involved, such as IL-18 [10], and that individuals may have distinct cytokine signatures depending on the type of CAD. The gene discussed is IL1B; the disease is coronary artery disorder.