STAT3 and glioblastoma: However, LC3‐II levels remained unchanged in ULK1 knockdown cells expressing the S727A mutant and treated with ULK1‐siRNA (Figure 7C), again demonstrating a key role of Y705 phosphorylation in the STAT3‐mediated suppression of autophagy via ULK1 signalling These studies suggest that autophagy induction by combining both STAT3 and ULK1 inhibition may be therapeutically beneficial for autophagy defective GBM cells.