Adult neurogenesis in the mammalian brain is mainly supported by neural stem cells (NSCs) located in the subventricular zone (SVZ) of the lateral ventricles. This process is regulated by specific extracellular and intracellular factors such as genomic imprinting (GI). GI is an epigenetic process that causes the monoallelic expression of a certain genes, called imprinted genes, being these expressed according to their parental origin. This phenomenon is controlled by epigenetic modifications at the imprinting control regions (ICR) that are differentially DNA methylated regions (DMRs) on the two parental chromosomes. Ten-eleven-translocation (TET) enzymes catalyze DNA demethylation, converting the 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC). Although 5hmC levels are high in the mouse brain, the potential role of TET proteins in regulating GI by controlling the methylation status of ICRs has not been described in adult neurogenesis. In the present work, we have characterized the role of Tet2 in adult neurogenesis by generating a conditional mouse model deficient in Tet2 specifically in NSCs. Furthermore, by genome-wide transcriptional and DNA methylation analysis, we characterized the TET2-modulated gene expression landscape in NSCs to understand the mechanisms underlying adult NSCs differentiation and how imprinted genes are affecting this process.