We appreciate the interest and comments from Drs De Rosa and Indolfi in regard to our article. 1 As stated in our article, neoatherosclerosis, which leads to late neointima formation, is seen across all 3 generations of metallic stents. It is our impression that the neointima of second-generation drug-eluting stents (DES) is less vulnerable and, as a result, associated with fewer events when compared with first-generation DES. Although vessel caging is also common across the 3 generations of metal stents, it is only one component of the mechanism for restenosis. Neoatherosclerosis has been frequently implicated as the final pathway of late failure for both DES and bare-metal stents.2 This widespread occurrence of neoatherosclerosis across stent generations may in fact explain the similarities in clinical presentation of in-stent restenosis and lead to the vulnerable stent. It remains to be seen whether neoatherosclerosis is independently associated with stent type and whether it carries an equal risk of vulnerability across stent generations.Imaging studies have shown that neoatherosclerosis occurs less frequently in second-than first-generation DES. Lee et al observed a lower rate of neoatherosclerosis in first-than secondgeneration DES, 3 and Yonetsu et al also demonstrated by univariable analysis that first-generation DES were significantly associated with neoatherosclerosis, whereas second-generation devices were not. 4 Furthermore, neointimal rupture is less likely to occur in patients with second-than first-generation DES.