APOA1 and coronary artery disorder: Many naturally occurring and bioengineered mutations (Table 2; Brouillette and Anantharamaiah, 1995; Sorci-Thomas and Thomas, 2002) and posttranslational modifications (Smith, 2010; Rosenson et al., 2016) in apoA-I have been reported and shown to alter HDL function or make it dysfunctional (e.g., by chlorination, oxidation, or nitration of specific apoA-I residues), resulting in impaired cholesterol efflux, change in HDL phenotype, and increased risk of coronary artery disease (CAD; Rosenson et al., 2016).