In addition, ChIP-qPCR and hMeDIP assays provided direct evidence that the reduced BCL2 expression in the hippocampus of fluoride-treated mice is attributable to the change of 5hmC level around the TSS of Bcl2. Therefore, the present comprehensive mechanistic study elucidating the involvement of TET1 in modulating BCL2 expression against neural apoptosis through increasing DNA hydroxymethylation will provide a novel therapeutic target for addressing prenatal fluoride-induced cognitive impairments. Here, BCL2 is linked to Cognitive impairment.