Functional analysis of the BCAA-raising gene signatures revealed that the causal effect might 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. Here, TRMT61A is linked to neuroendocrine disorder.