Therapies that suppress the circulating concentration of the respective amyloid fibril precursor protein reduce the substrate available required for new amyloid formation.1 In the case of ATTR amyloidosis, ongoing amyloid formation can also be inhibited by drugs that stabilize the normal soluble TTR tetramer, thereby reducing the availability of misfolded TTR species that serve as the substrate for ATTR amyloid fibril formation.7 There are currently no biological assays that specifically measure the rate of amyloid formation or the rate of amyloid clearance in vivo. Here, TTR is linked to amyloidosis.