Eukaryotes from yeast to humans employ heterochromatin, a compact chromatin structure, to stably silence gene expression and ultimately influence cellular identity and genomic integrity. In the budding yeast Saccharomyces cerevisiae, the Silent Information Regulator (SIR) proteins impart heterochromatic silencing at the silent mating-type loci HML and HMR. Silencing at HML and HMR leads to a 1000-fold reduction in transcription over the expressed state, is stably inherited from mother to daughter cell, and is critical for maintaining haploid identity. Our lab recently developed a novel assay to capture the dynamics of heterochromatic silencing in budding yeast, which we have named the Cre-Reported Altered States of Heterochromatin, or CRASH, assay. We placed the cre recombinase gene at the HML locus to monitor heterochromatin stability. Lapses in silencing at HML allow Cre to excise a loxP-flanked RFP cassette, subsequently activating GFP expression and revealing for the first time rare and transient silencing losses in wild-type cells. In this study, we exploited the sensitivity of the CRASH assay to understand how homologous recombination within the silent HML locus impacts its ability to remain transcriptionally silent. Recombination within heterochromatin requires access to an otherwise occlusive chromatin structure, yet whether this invasive process also disrupts silencing is unknown. We introduced into cells equipped with the CRASH assay a double-strand break that induces homology-directed repair from HML. Interestingly, our results demonstrate that homologous recombination can occur in a heterochromatic donor without an obligate loss of silencing. However, it appears that many cells that template recombination at HML lose transcriptional silencing in the process. The reasons for these two distinct outcomes are under active investigation.