Amyloidosis is a systemic disorder marked by extracellular deposition of insoluble β-sheet fibrillar proteins, resistant to proteolytic cleavage, causing progressive organ dysfunction.3,4 Over 30 precursor proteins are implicated in amyloid formation, often associated with proteoglycans and serum amyloid P.4 Among these, cardiac involvement stands as the most critical prognostic factor, predominantly driven by two protein types: immunoglobulin-derived light chains (amyloid light-chain cardiac amyloidosis) and transthyretin (transthyretin cardiac amyloidosis). This evidence concerns the gene TTR and amyloidosis.