In this context, our findings demonstrating a reduction in size and cellularity of advanced lesions in mice with bone marrow specific deficiency of α7nAChR provide novel experimental evidence underscoring a potential role of macrophage α7nAChR in advanced atherosclerosis and set a framework for future studies aimed at characterizing the mechanisms coupling α7nAChR signaling to macrophage function in atherosclerosis. This evidence concerns the gene CHRNA7 and atherosclerosis.