Collectively, these results suggested that high circulating BCAA levels can influence CAD and subsequent plaque rupture events via two distinct pathways: glucose metabolism disorder (as shown by PPM1K and TRMT61A) through processes leading to chronic vulnerability to CAD and neuroendocrine dysregulation (as shown by CBLN1, MRL33, and C2orf16) affecting hemodynamic factors and platelets through neuroendocrine factors, which in turn affect subsequent plaque rupture and thrombosis in CAD, triggering ischemic events. This evidence concerns the gene PPM1K and glucose metabolism disease.