A single center cohort study conducted by Stallone and colleagues [32] proved intense interaction between C1q and PTX-3, increased expressions of two anaphylatoxins (C3a and C5a receptors) and tissular complement inhibitor CD59 in patients diagnosed with prostatic cancer while no interactions were noted in those diagnosed with prostatic benign hyperplasia. The gene discussed is CD59; the disease is Familial prostate cancer.