Accumulating evidence suggests that apoA-I plays a critical role not only in maintaining normal endothelial function [25], [26] but also in protecting cardiomyocytes from various types of insults including ischemic and re-perfusion injury [11], doxorubicin induced cardiomyocytes [10], and diabetic cardiomyopathy [12] through alternative mechanisms unrelated to cholesterol transportation. This evidence concerns the gene APOA1 and diabetic cardiomyopathy.