As the pro-inflammatory cytokine IL-18 is a downstream product of both pathways [32, 33] (the NLRP3 inflammasome also capable of activating NF-ΚB directly [34]), SIRT1 expression might have been downregulated in EAT, with respect to the observed lowest expression in EAT and the strong and inverse correlation between SIRT1 and IL-18 in EAT in our CHD population, and the previously reported significantly elevated IL-18 expression levels in EAT compared to PAT and SAT in the same cohort [5]. The gene discussed is IL18; the disease is coronary artery disorder.