However, removing Cul4b, specifically, in the germ cell population does not lead to this phenotype, despite spermiogenesis defects and male sterility; because Cul4a is not expressed in the adult spermatogonia, the distinctive male infertility phenotypes present in the global and germ cell-specific Cul4b–null mutants prompted us to speculate that a non-cell autonomous mechanism is responsible for CUL4B-mediated SSC maintenance. Here, CUL4B is linked to male infertility.