To assess whether ageing and dilated cardiomyopathy (DCM) potentiate p16‐STAT3 interaction, our comparative analysis revealed that young‐healthy controls exhibited a significantly lower abundance of p16‐positive cells and p16/STAT3 co‐expressing cells compared to old‐healthy individuals, whereas old‐DCM patients showed marked increases in these populations (Figure 4G–I). Here, CDKN2A is linked to familial dilated cardiomyopathy.