Until the end of the last century, it was thought that this ability was limited to around 20 proteins, identified as the main constituents of the amyloid deposits observed in well-defined pathological conditions, including Alzheimer’s disease (AD), Parkinson’s disease (PD), light chain amyloidosis (AL) and transthyretin amyloidosis (ATTR) [4,5]. This evidence concerns the gene TTR and axial length measurement.