The TET dioxygenases mediate DNA demethylation in pre-implantation embryos and in primordial germ cells, yet limited studies address their contribution to the global gain of DNA methylation following implantation. Here, we discuss our recent study revealing that Tet1 is expressed and functions non-redundantly in the early post-implantation mouse embryo. Ablating TET1 affects the methylation status of primed epiblast cells; however, the majority of gene expression regulation by TET1 seems to be independent of any gain or loss in methylation/hydroxymethylation due to TET1 omission. Interestingly, we reveal a gene repressive effect of TET1. Moreover, we show that loss of TET1 leads to developmental defects resulting in embryonic lethality with different penetrance depending on the genetic background of the mice.