CDKN1A encodes p21, a potent cyclin-dependent kinase inhibitor that has been reported to have dual effects in breast cancer as both a key mediator of p53-dependent cell cycle arrest and an inhibitor of cell apoptosis.51,52 p21 has also been shown to mediate postnatal cardiomyocyte cell cycle arrest, facilitate the development of cardiac hypertrophy, and regulate LPS-induced cardiac dysfunction.53–55 Our findings suggest a potential dual role of CDKN1A across breast cancer and CAD, warrant further functional validation to elucidate potential mechanisms contributing to both conditions. Here, TP53 is linked to cardiac hypertrophy.