This study investigates how the protein KMT5C uses structural disorder to work together with HP1 proteins to maintain heterochromatin, a tightly packed form of DNA important for gene regulation. While the full abstract is not available, this research is relevant to understanding chromatin organization, which is disrupted in conditions like White-Sutton syndrome caused by variants in POGZ — a protein that also interacts with HP1. Understanding these molecular partnerships may shed light on how gene silencing goes wrong in neurodevelopmental disorders.