On the basis of the molecular structure of the amyloid deposits, it is possible to distinguish three main etiologies of CA, which together account for approximately 98% of clinical cases [2]: primary light chain (AL) amyloidosis, hereditary transthyretin (ATTRv; v = variant) and wild-type transthyretin (ATTRwt) amyloidosis. This evidence concerns the gene TTR and amyloidosis.