Importantly, our ChIP-qPCR and hMeDIP assays further provided direct evidence that the reduced expression of BCL2 in the hippocampus of fluoride-treated mice was attributable to alterations in the 5hmC level around the TSS of Bcl2. On the basis of our present bioinformatic analysis of CpG islands of Bcl2 in combination with sequential oxidation of 5-mC to 5-hydroxymethylcytosine (5-hmC) by TET enzymes, we speculated that TET1 mitigates prenatal fluoride-induced cognitive impairment by modulating the DNA hydroxymethylation of Bcl2, leading to its up-regulation. The gene discussed is BCL2; the disease is Cognitive impairment.