Indeed, previous studies have shown that AKT can regulated SOX2 expression in non-small lung cancers33 and enhanced SOX2 protein levels in hippocampal neural progenitor cells.34 Besides, our previous study had reported that AKT phosphorylates SOX2 at T116 and blocks the interaction of SOX2 with UBR5, which protects SOX2 from ubiquitin-dependent protein degradation by UBR5 in human esophageal cancer.16 It worth noting that it exits not identical mechanism of AKT-mediated SOX2 stability in OS cells. The gene discussed is UBR5; the disease is esophageal cancer.