TTR appears to function as a molecularchaperone in preventing amyloid formation of Aβ in the brain1−4 and islet amyloid polypeptide (IAPP) in the pancreas.5 TTR is inherently amyloidogenic, and the wild-typeprotein accounts for a significant number of cardiac amyloidosis casesin elderly people6 as well as diverse mutation-dependentamyloid disease phenotypes in familial diseases such as familial amyloidpolyneuropathy (FAP).7 Collectively thisgroup of diseases are known as transthyretin amyloidosis with depositedATTR. Here, IAPP is linked to cardiac amyloidosis.