The exact mechanism of hyperglycemia-induced enhancement of CD36 and ACAT-1 remains unknown; however, hyperglycemia-mediated accumulation of reactive oxygen species has the possibility to induce proinflammatory signaling, including p38 mitogen-activated protein kinase, leading to the induction of the nuclear transcription factor-kappaB (NF-κB) signaling pathway and subsequent increase in CD36 expression [15]. This evidence concerns the gene ACAT1 and Hyperglycemia.