SAA1 and amyloidosis: 2014). The liver synthesizes SAA in response to inflammation, in which it can enhance the antioxidant potential of HDL cholesterol (Sato et al. 2016; Sun and Ye 2016). However, the misfolding of the N-terminus region of SAA can lead to amyloidosis, which is the accumulation of pathogenic misfolded protein amyloid in targeted tissue(s) (Westermark et al. 2015; Gaffney 2017). The aggregation and subsequent accumulation of amyloid occurs when these fibrillar peptides misfold into secondary structures, rich in ß-sheets (Real de Asua et al. 2014; Westermark et al. 2015).