Targeted clearance of p16Ink4 ‐expressing cells in p16‐INK‐ATTAC (p16Ink4a apoptosis through targeted activation of caspase) mice in the presence of AP20187 (a synthetic drug that dimerizes a membrane‐bound myristoylated FK506‐binding protein‐caspase‐8 [FKBP–Casp8] fusion protein) has been successfully used as a strategy to understand the effect of clearing p16Ink4a‐expressing senescent cells on multiple age‐related conditions, including osteoporosis, frailty, cardiovascular disease, and metabolic dysfunction (for reviews, see (Tchkonia et al., 2013) and (Khosla et al., 2020)). Here, CDKN2A is linked to cardiovascular disorder.