Most cases of amyloidosis originate either from excessive secretion of abnormal immunoglobulin light chains by clonal proliferation of plasma cells, termed light chain (AL) amyloidosis, or from dissociation and misfolding of transthyretin, a transporter protein for thyroxine and retinol-binding protein 4 complex, termed transthyretin (ATTR) amyloidosis.1,2. The gene discussed is RBP4; the disease is amyloidosis.