Both drugs can successfully complex to the thyroxine binding site and kinetically stabilize TTR tetramers, inhibiting the release of the TTR monomer required for amyloidogenesis.16, 17 Previous clinical trials among ATTRv‐PN patients have shown that diflunisal and tafamidis can reduce the progression of neurological impairment.13, 14 Additionally, tafamidis can reduce the number of cardiovascular‐related hospitalizations and the rate of all‐cause mortality in patients with cardiomyopathy related to TTR amyloidosis.18 This evidence concerns the gene TTR and amyloidosis.