Friedreich Ataxia is an inherited neurogenerative disorder caused by the expansion of intronic GAA/TTC repeats in the FXN gene. Repeat expansions in the intron affect the expression of the FXN gene associated with epigenetic changes. We discovered an intronic repeat expansion associated with a growth defect in the Arabidopsis thaliana. Intronic GAA/TTC triplet repeat expansion in the IIL1 locus affects its expression, similar to Friedreich Ataxia. We recently showed that repeat expansions induce small RNAs, which then trigger the RNA-dependent DNA Methylation (RdDM) pathway to cause gene silencing of the IIL1 locus. Here we have identified mutants that restored the IIL1 expression despite carrying long stretches of GAA/TTC repeat expansions. Next-generation sequencing-based positional cloning identified causal genes at nine loci, including a novel uncharacterized gene. Further characterization of this gene revealed a role for SUMOylation/deSUMOylation in the epigenetic silencing of expanded repeats. I will present our findings, which reveal the fundamental role of post-translational modifications in epigenetic silencing caused by repeat expansions.