Overall, the causal effect may involve two pathophysiological pathways, including glucose metabolism (PPM1K and TRMT61A) related to plaque progression and the newly discovered neuroendocrine disorders (CBLN1, MRPL33, and C2orf16) related to plaque rupture and thrombosis (Figure 4). The gene discussed is SPATA31H1; the disease is neuroendocrine disorder.