Ding et al. (2021) found that the absence of SIRT3 led to increased cholesterol accumulation, oxidative stress, and activation of the NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) in ox-LDL-stimulated macrophages, thereby promoting foam cell formation. This highlights SIRT3 as an effective target for anti-atherosclerosis therapy. Moreover, research indicates that DHM can effectively inhibit this process through a SIRT3-dependent mechanism, demonstrating promising anti-atherosclerosis effects (Ding et al., 2021). This evidence concerns the gene SIRT3 and atherosclerosis.