Zhang and colleagues also uncovered a novel SE-driven transcription mechanism involving FOSL1 as a key regulator within the AP-1 complex, which predominantly functions via selective associations with mediators to establish super-enhancers at a cohort of cancer stemness and pro-metastatic genes, such as SNAI2 and FOSL1 itself, thereby promoting tumor initiation and metastasis in HNSCC.75 The gene discussed is SNAI2; the disease is neoplasm.