APOA1 and atherosclerosis: Investigating the susceptibility of apoA-I to oxidative damage at sites of inflammation can help understand how dysfunctional HDL emerges (DiDonato et al., 2013, 2014; Huang et al., 2013, 2014), and should lead to better ways to shield apoA-I from chemical alteration, and to efficient therapeutic approaches for treating atherosclerosis.