The N-terminal fragment, essential for the stabilization of the secondary structure of ApoA1 [200], is generally highly conserved in apolipoprotein-derived amyloidosis and seems to have an important role in the formation of amyloid fibrils [190,201,202,203,204], in particular in those amyloidosis affecting patients with chronic inflammatory disorders (secondary or reactive amyloidosis) [205]. Here, APOA1 is linked to amyloidosis.