While the misfolding, accumulation and deposit of immunoglobulin light chains (monoclonal kappa or lambda) lead to AL CA [3], amyloid formation and deposition in transthyretin amyloidosis results from dissociation of the tetrameric transthyretin molecule (due either to a genetic mutation, ATTRv, or ageing in ATTRwt) and the misfolding of the resulting monomers into amyloid fibrils [4]. This evidence concerns the gene TTR and axial length measurement.