Enhanced miR-155 levels with CHD severity could additionally increase pro-inflammatory mediator generation, causing endothelial cell dysfunction and apoptosis; and altering toll-like receptor (TLR), angiotensin II and Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signalling [47–49], whilst further disrupting other key responses in smooth muscle cells [50, 51]. This evidence concerns the gene AGT and coronary artery disorder.