The anti-inflammatory effects of Faecalibacterium prausnitzii are predominantly reflected in the inhibition of the release of inflammatory cytokines, including interleukins, tumor necrosis factors, and interferons, and the suppression of inflammatory-related pathways, such as NF-κB pathway and NLRP3 pathway, which are the primary pathological mechanism of CAD as well [182, 183]. This evidence concerns the gene NLRP3 and coronary artery disorder.