It recently has been reported that because the FR is a marker of macrophage activation, FR-expressing macrophages represent a specific target for folate-linked drugs, given that they would not be taken up by nonactivated macrophages.14 It also has been reported that macrophages taking up folate accumulate in the atherosclerotic lesions of apolipoprotein E (apoE)–deficient mice.15 We therefore hypothesized that depletion of FRβ-expressing macrophages via the dsFv anti–FRβ-PE38 immunotoxin could be beneficial in treating atherosclerosis by specifically targeting activated macrophages. This evidence concerns the gene FOLR2 and atherosclerosis.