The reasons which led us to choose spermatogenesis and testicular cancer to study CCDC6 include: (i) that CCDC6 is predicted as downregulated in germ cell tumours (by the analysis of the ArrayExpress Archive database), (ii) the occurrence, in the same tissue, of both mitotic and meiotic cell cycles, (iii) the high frequency of programmed DSBs as an essential part of genetic recombination during meiosis and (iv) the oxidative DNA damage envisaged as emerging mechanism of carcinogenesis in this tissue [5,34]. Here, CCDC6 is linked to testicular cancer.