Sex differences in the brain are typically attributed to sex chromosome complement, as well as to the organizational and activational effects of gonadal steroids. In rodents, males—but not females—undergo perinatal surges of testosterone that influence developmental processes such as cell death, neuronal survival, and dendritic growth; ultimately leading to morphological sex differences. We previously showed that the neonatal epigenome is sexually differentiated early in life: male mice exhibit higher expression of DNA demethylation enzymes in the prefrontal cortex (PFC) during the critical period of sexual differentiation, along with greater oxytocin receptor (OTR) expression at postnatal day (P)7 compared to females. These findings suggest that precise regulation of DNA methylation programs sexual differentiation of the rodent brain. Here, we investigate whether testosterone regulates early sex differences in the mRNA expression of Tet1-3, Gadd45a/b, and Tdg (enzymes involved in 5-methylcytosine removal), and whether this regulation correlates with OTR expression in the developing brain. Preliminary results suggest that neonatal testosterone treatment in females induces expression patterns resembling those of males. Thus, testosterone-dependent programming of DNA methylation and demethylation may contribute to sex-specific OTR expression and underlie broader epigenetic mechanisms of brain sexual differentiation.