Of course, we cannot rule out that other oncogenic factors (KRAS), TFs (p53), or epigenetic modifiers (UTX) are also involved in LIF transcription in HNSCC as reported among other biological contexts.[26, 49, 50] In aggregate, we conclude that SOX2 and SMAD3 bind to LIF‐SE to activate LIF transcription and thereby facilitate CSC maintenance and tumor development in HNSCC. The gene discussed is KRAS; the disease is neoplasm.