SOAT1 and neoplasm: In support of this idea, knock-down of STAT1 predisposed nu61 HNSCC cells to RT-driven suppression of glycolysis and reduction in anti-oxidation capacity, leading to greater tumor growth suppression and radiosensitization [67], but it remains to be tested how IOs affect STAT1 and other members of the JAK-STAT family in tumor cells.