TMAO can contribute to the development of heart failure by promoting an inflammatory state with elevated values of cytokines such as Interleukins 6 and 1 (IL-6, IL-1), Tumor Necrosis factor-α (TNF-α), oxidative stress, and endothelial dysfunction and by increasing oxygen consumption, which alters cardiac metabolism in patients with heart failure [42]. This evidence concerns the gene IL16 and heart failure.