In our study, aa 36–48 is significantly less common than aa 22–34, suggesting that all cases are likely to be ATTR type A. Ihse et al. reported that patients with ATTR fragments (type A) have a late onset of amyloidosis and are more likely to develop cardiomyopathy, while patients without fragments (type B) have an early onset of amyloidosis with a higher incidence of neuropathy and a lower incidence of myocardial involvement [9]. The gene discussed is TTR; the disease is amyloidosis.