While much is established about the chromatin occupancy (e.g., mainly at gene promoters and enhancers), deposition mechanisms (e.g., by p400 and SWI2–SNF2-related CBP activator protein (SRCAP)) and posttranslational modification (e.g., acetylation) of H2AZ, as well as its effect on chromatin structure and gene transcription (e.g., destabilizes nucleosomes and facilitates gene transcription), how H2AZ is dysregulated in cancer remains poorly understood [14, 17–23]. The gene discussed is SRCAP; the disease is cancer.