Senescence can be induced by various cellular stimuli, many of which involve the activation of p53 and its consequential activation of cyclin‐dependent kinase (CDK) inhibitors, such as p16 (also known as INK4A), p15 (also known as INK4B), p21 (also known as WAF1) and p27.29, 30 Therefore, senescence is becoming a promising treatment to combat the progression of cancer.31, 32. This evidence concerns the gene CDKN2B and cancer.