Homocysteine has been shown to contribute to dyslipidemia via pathological activation of the sterol regulatory element-binding proteins, thus contributing to cardiovascular disease (21); DTT is a reducing agent capable of preventing disulfide bond formation of nascent proteins in the ER by chaperones such as protein disulfide isomerase and ERp72 (22); and bisphenol-A is an estrogen mimetic commonly found in plastics, capable of antagonizing the SERCA pump in a manner similar to TG (23). Here, CNBP is linked to cardiovascular disorder.