Functional analysis of the BCAA-raising genes suggested the causal involvement of two pathophysiological pathways, including glucose metabolism (PPM1K and TRMT61A) related to plaque progression, and the newly discovered neuroendocrine disorders regulating blood pressure (MRPL33, CBLN1, and C2orf16) related to plaque rupture and thrombosis. Here, MRPL33 is linked to neuroendocrine disorder.