Double strand breaks (DSBs) are arguably the most deleterious DNA lesion that a cell can sustain, and defects in the ability to detect and repair these breaks result in increased genomic instability and have been causatively linked to cancer. The repair of DNA DSBs must occur in the context of chromatin, and there is increasing evidence that the modulation of chromatin plays an integral role in the DNA DSB repair process. Here, we summarize a number of key findings, largely from studies performed in budding yeast, highlighting the role of chromatin in DNA DSB responses.