While TTR has been linked to amyloidosis, both wt-TTRand the T119M mutant protect against amyloid-β toxicity.1 L55P and V30M mutations of TTR tend to increaserates of aggregation in organs such as the heart and kidneys,2−4 whereas F87A and T119M mutations reduce the amyloidogenic natureof TTR.5,6 Heterozygous individuals express both wt-TTRand mTTR subunits, which give rise to hybrid TTR (hTTR) tetramersthat have also been linked to amyloidosis. This evidence concerns the gene MT-TR and amyloidosis.