Recently, SOX2 has also been reported to play a key role in HNSCC immune escape.38,39 In a study conducted on immunocompetent mice, SOX2 expression in HNSCC tumor cells decreased CD8+ T-lymphocyte infiltration and promoted tumor growth through suppression of stimulation of interferon genes (STING)-dependent interferon-I-mediated signaling. The gene discussed is SOX2; the disease is neoplasm.