CAD-DM2 patients had less beneficial or commensal bacteria (such as Faecalibacterium prausnitzii, and Bacteroides fragilis) and more opportunistic pathogens (such as Enterobacteriaceae, Streptococcus, and Desulfovibrio) that may impair intestinal barrier function (increasing zonulin levels), enhance the serum levels of TMAO, and may therefore contribute to inflammatory processes related to CAD by means of increasing the production of inflammatory cytokines (such as IL-1B). This evidence concerns the gene IL1B and coronary artery disorder.