This suggests that increased secretion of nontetrameric TTR from the liver—the primary site of TTR synthesis—could exacerbate protein aggregation in the blood and contribute to the increased population of nonnative TTR observed in plasma collected from TTR amyloid disease patients suffering from polyneuropathy (Schonhoft et al., 2017; Jiang et al., 2021). The gene discussed is TTR; the disease is polyneuropathy.