These studies do not only indicate that the epigenetic postnatal stability of the DNA methylation of AhRR at 18 months is a mediator for long-term impacts in humans due to prenatal exposure to toxins [104], but also suggest DNA hypomethylation in the early development period can persist for a long period, and indicate possibility of AhR/CYP1A1 causing autism in individuals facilitated by the hypomethylation of its repressor gene by environmental toxins. This evidence concerns the gene AHR and autism.