It is intriguing that in our study, activated p-Akt reduced P-GSK3β (Ser9) but increased p-FOXOs, which is different from the case in hepatocellular carcinoma where p-Akt increased P-GSK3β (Ser9) and p-FOXOs; concomitantly, this difference makes that active GSK3β in our study can not upregulate IGF-1R expression by FOXO1a and FOXO3a binding to IGF-1R promoter [33]. The gene discussed is GSK3B; the disease is hepatocellular carcinoma.