The extent of nerve fiber loss is more conspicuous, despite the smaller number of amyloid deposits, in late-onset ATTRv amyloidosis patients from non-endemic areas than in early-onset ATTRv amyloidosis patients from endemic foci [4], suggesting that the toxicity of non-fibrillar TTR participates in the mechanisms of neurodegeneration, especially in late-onset ATTRv amyloidosis patients from non-endemic areas. This evidence concerns the gene TTR and amyloidosis.