The precursor proteins involved in protein misfolding diseases (PMDs), however, are considerably different in their native states and range from disordered proteins (e.g., amyloid-beta – Aβ – in AD, α-synuclein – αSyn – in PD, the prion protein in prion disease) to structured monomers (e.g., beta-2 microglobulin – β2m – in β2m-amyloidosis) or globular oligomers (the transthyretin – TTR – tetramer in TTR-amyloidosis). This evidence concerns the gene B2M and amyloidosis.