As large-scale entropy represents vascular regulatory function, the finding is consistent with that of a previous study demonstrating that the cellular and molecular mechanisms underlying hypercholesterolemia could contribute to an imbalance between phosphorylation and dephosphorylation of lipid and protein kinase, thereby modulating vascular endothelial L-arginine/nitric oxide synthetase (eNOS) and produce vascular endothelium dysfunction [36]. This evidence concerns the gene WEE1 and familial hypercholesterolemia.