DNA methylation is an epigenetic mechanism that promotes heterochromatin formation, silences imprinted loci, the X chromosome, repeats and transposable elements. The idea that DNA methylation also represses differentially expressed genes has been challenged by experiments showing that loss of genomic methylation, either during early embryonic development or in mutants, does not result in a burst of gene activation. On p. 2925, work by Kirsten Sadler and co-workers confirms and extends the model that DNA methylation functions primarily as a gatekeeper for transposons. They report that mutants with a hypomethylated genome upregulate interferons, leading to the recruitment and expansion of immune cells in the developing larva. Rather than being directly due to derepression of interferon genes in the demethylated state, interferon production is stimulated by the detection of nucleic acids in the cytosol of a cell. This normally indicates the presence of a virus, but the mutants used in the study were not infected. So, what elicits this response? The authors reveal that the aberrant transcription of transposable elements caused by demethylation results in the production of cytosolic DNA that triggers the antiviral response. This mechanism could act as an early-warning system, allowing cells in the developing embryo with widespread epigenetic abnormalities to be put under immune surveillance so they can be rapidly eliminated if necessary.