It is widely known that TTR protein destabilized by TTR gene mutation has a tendency to dissociate into monomers, which then misfold and aggregate into amyloid fibrils, leading to autosomal-dominant hereditary amyloidosis, including familial amyloid polyneuropathy (FAP), familial amyloid cardiomyopathy (FAC), and familial leptomeningeal amyloidosis. The gene discussed is TTR; the disease is amyloidosis.