Conversions between two epigenetically heritable states (fully active or silent) are regulated by chromatin and integral for development and disease. The mechanisms of epigenetic conversions are not fully elucidated. CAF-I and Rrm3p are key regulators of conversions. I hypothesized that the kinases Cdc7p and Cdc28p phosphorylate CAF-I and facilitate its association with PCNA. Both CAF-I and Rrm3p interact with PCNA through the same domain. Therefore, I hypothesized that CAF-I and Rrm3p compete for PCNA. I used a modified yeast two-hybrid assay to assess the CAF-I/PCNA interaction. This interaction was significantly reduced when Cdc7p phosphorylation of Cac1p is prevented. I used a similar assay to show that CAF-I and Rrm3p compete for PCNA. I also showed differential binding between Cac1p and Rrm3p, which indicated that the PIP box is not the only motif responsible for the interaction. Finally, I proposed and discussed a new model for such conversions.