Our results identify a unique apoptosis-resistant, lipid-prone, and non-inflammatory Mac3+Mafb+AIM+ subset that contributes to AT progression; the relation of this subset to subsets previously reported in the atherosclerotic plaque (Mox, M(Hem), M(Hb), and M4)5 deserves further analysis. Here, CD5L is linked to ataxia telangiectasia.