Transthyretin (ATTR) amyloidosis is a systemic disorder particularly affecting the heart and nerves resulting from the misfolding and aggregation of transthyretin (TTR) protein into amyloid fibrils. Cardiac amyloidosis can lead to debilitating heart failure, arrhythmias, and poor survival, with a median life expectancy of 2–6 years following diagnosis (1). Although TTR stabilisers like tafamidis have been demonstrated to slow disease progression, emerging gene-silencing therapies are revolutionising the treatment landscape (2,3) . These therapies target TTR protein production at the genetic level, providing more potent disease modification. The recently completed HELIOS-B trial highlights the efficacy of a gene silencer, vutrisiran, in ATTR amyloidosis and cardiomyopathy, advancing hopes for improved outcomes in this challenging condition (4).