Recently, we demonstrated compensatory functions of HDAC1 and HDAC2 during mouse oocyte development in which Hdac1 and Hdac2 were specifically deleted in oocytes [14]; deletion of both genes in oocytes results in infertility due to failure of follicle development beyond the secondary follicle stage with ensuing oocyte apoptosis attributed to hyperaceytlation of TRP53. The gene discussed is HDAC1; the disease is Infertility.