However, in atherosclerosis, ox-LDL and cholesterol crystallization in the plaque will continuously activate NLRP3 inflammatory bodies and caspase-1, resulting in a continuous increase in the release of inflammatory factors, thus promoting the enhancement of inflammatory response in the atherosclerotic region and reducing the stability of the plaque (Hoseini et al., 2018) (Figure 3). This evidence concerns the gene NLRP3 and atherosclerosis.