Inhibition of NF‐κB activity can effectively alleviate or delay cell senescence.[9] In many age‐related diseases, such as atherosclerosis and diabetes, NF‐κB is continuously activated.[10] As a key mediator in the inflammasome family, NOD‐like receptor protein 3 (NLRP3) can be activated by a series of danger signals such as metabolic wastes, stress stimuli, and internal and external harmful metabolites. The gene discussed is NFKB1; the disease is atherosclerosis.