This is further witnessed by the progression of cardiac amyloidosis despite the almost complete removal of variant TTR from the circulation in ATTRv patients undergoing liver transplantation—a sort of surgical gene therapy that has represented the only therapeutic option for selected patients with ATTRv for decades—which is explained by the continuous deposition of wild-type TTR in the myocardium [45,46]. The gene discussed is TTR; the disease is cardiac amyloidosis.