After recovery from stress by pests and diseases, plants maintain an elevated state of defence. This induced resistance (IR) is often based on defence priming, which enables a faster and stronger immune response upon recurrent exposure to the same type of attacker. We study the epigenetic basis of this form of immune memory. We have recently shown that exposure of seedlings to herbivory induces long-lasting DNA de-methylation at transposable elements (TEs), which prime genomically distant defence genes. Although more variable in intensity, immune memory can partially be transmitted to the offspring of stressed plants. This heritable IR is proportional to the stress encountered in previous generations and involves the DNA demethylase ROS1. To advance our understanding of how DNA demethylation controls immune memory, we are following artificial strategies to manipulate the plant methylome. Using epigenetic recombinant inbred lines (epiRILs), which share the same genetic (wild-type) background but vary in heritable DNA methylation of TE-rich regions, we have previously identified epialleles that prime defence gene expression and provide high levels of disease resistance without negative effects on plant growth. To translate this form of epigenetic disease resistance to crops, we are currently developing a new method to introduce dosed amounts of ROS1-dependent DNA hypo-methylation into plant genomes. This tool will not only allow us to induce long-lasting resistance against pests and diseases, but also explore the epigenetic mechanisms by which plants establish, maintain and reset immune memory.