Researchers have explored the treatment of periodontitis by promoting M2 polarization of macrophages through the inhibition of the Akt2/JNK/c-Jun and Akt2/miR-155-5p/DET1/c-Jun signaling pathways.25 Additionally, some studies have investigated increasing the number of M2 macrophages by delivering microparticles carrying CCL2 as a therapeutic strategy for periodontitis.26 Given that macrophages highly express the C3aR, it is reasonably hypothesized that the C3a promotes periodontal tissue inflammation in periodontitis mice by mediating the polarization of macrophages. The gene discussed is JUN; the disease is periodontitis.