This may be due to the following reasons: (a) higher endogenous estrogen levels in female offspring partly normalize the testosterone effect of LNG; (b) the female offspring have a higher basal expression of ERβ compared to male offspring, which is more resistant to LNG-induced ERβ suppression; and (c) higher estrogen levels in female offspring could activate ERβ and upregulate its target genes SOD2 and ERRα and subsequently ameliorate tissue damage [15, 16] with less responsiveness to autism-like behavior development. This evidence concerns the gene ESR2 and autism.