The formation and inhibited emigration of foam cells are the key events in malignant remodeling of artery plaques. Advanced glycation end products (AGE) play an important role in the course of diabetes-accelerating atherosclerotic progression. Based on the latest international research progress and our existing results, this paper elaborated the mechanism of CD36 modulating foam cell emigration from plaques inhibited by Nε-carboxymethyl-Lysine, which would provide a new starting point for the treatment strategy of targeting foam cell migration mechanism in the future.