For instance, deficiency of ten-eleven translocation (TET) proteins, specifically TET1 and TET2, resulted in increased DNA methylation because of the abnormal conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), ultimately leading to declined follicle reserve and premature ovarian failure [59, 60]. The gene discussed is TET1; the disease is primary ovarian failure.