C3a-C3aR signalling in fibroblasts is thought to lead to their activation and subsequent upregulation of pro-tumorigenic cytokines such as transforming growth factor β (TGF-β) and the promotion of lung metastasis via EMT, as C3aR deficiency or pharmacological blockade decrease TGF-β expression, EMT, and thus metastasis in a mouse breast cancer model (Figure 1). The gene discussed is C3; the disease is breast cancer.