Moreover, expression of TRIM56 and IFNGR1, which both act as mediators of immune dysregulation by activating the cGAS‐STING signalling pathway,48, 49 a critical driver of ageing‐related inflammation50 and known to contribute to adverse left ventricular remodelling leading to heart failure in mice,51 were specifically up‐regulated in LOY monocytes of patients simultaneously harbouring DNMT3A CHIP‐driver mutations. Here, TRIM56 is linked to heart failure.