Data from other studies support the notion that mechanisms that limit complement activation could improve the anti-tumor effect of radiotherapy, although in contrast, Surace et al. found that interfering with the anaphylatoxins C3a and C5a reduced the efficacy of radiotherapy in murine melanoma, colon cancer, and human skin cancer models indicating that a systemic functionally active complement system yields high anti-tumor potential [29]. The gene discussed is C3; the disease is skin cancer.