Both in the tamoxifen inducible (iKO) and in the constitutive Ngn3-Cre driven (sKO) deletion models, we observed that differentiating spermatogonia were highly susceptible to Kdm2a deficiency, as reflected by reduced numbers of c-KIT-positive spermatogonia, delayed progression through the cell cycle of intermediate and B spermatogonia, and increased apoptosis resulting in severe spermatogenic defects and infertility. The gene discussed is KDM2A; the disease is Infertility.