44 Our model does have some limitations, which are common with other methods utilizing sections with the stent remaining in situ. The thickness of the stent sections obtained, along with the fact that the spiral coil stent rises out of the tissue in each section, leads to a difﬁculty in obtaining high-quality images. In addition, immunohis- tochemical staining is limited in tissue embedded in methylmetha- crylate resin, which is further exacerbated by the thickness of the section obtained. This limits the ability to characterize events causing in-stent restenosis in this model and could limit its usefulness to investigations of efﬁcacy of potential treatments. However, despite the limitations on immunostaining, we have managed to achieve positive staining for smooth muscle, inﬂammatory and endo- thelial cells, depending on the methylmethacrylate resin used, antigen retrieval, and an altered incubation protocol from the stan- dard used with wax-embedded sections. The usefulness of this model in interventional studies is shown by the response to stenting of mice deﬁcient in IL-1 signalling, com- pared with wild-type mice. We have previously shown that these mice develop a signiﬁcantly reduced neointima in response to carotid ligation injury,6 a response that is duplicated using our stent model. Bone marrow transplant experiments in these mice suggest IL-1 signalling in both vascular wall cells and circulating (inﬂammatory and progenitor) cells play an equal role in neointima formation following carotid ligation,6 and it is likely that the same mechanism is involved in in-stent restenosis, following stenting of these mice. In conclusion, we have established a new model of in situ murine stenting. The model mimics features of neointimal formation in the human, and replicates those of other animal stent models. 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