Cardiac amyloidosis encountered in clinical practice is in the vast majority of cases caused by light chain (AL) or transthyretin amyloidosis (ATTR), with the latter consisting of two subtypes: Senile ATTR amyloidosis, which is caused by wild-type transthyretin deposition (ATTRwt), and familial ATTR amyloidosis, which is caused by mutant proteins that exhibit increased fibrillogenicity (ATTRm or ATTRv, where ‘v’ stems from ‘variant’) [1, 3, 4]. This evidence concerns the gene TTR and axial length measurement.