Although clinical evaluations indicated that progression of other clinical symptoms such as peripheral neuropathy [73,74], GI symptoms [75], and renal involvement [72,76] usually stopped after LT in FAP ATTR Val30Met patients, other studies suggested that LT failed to prevent progression of cardiac amyloidosis in FAP ATTR Val30Met patients after LT [69,77], with this failure reportedly being due to continued formation of amyloid mainly derived from WT TTR secreted from the transplanted normal liver graft [29,30,78]. This evidence concerns the gene FAP and cardiac amyloidosis.