However, on the other hand, PI3K-AKT-activated disassociation of a transcription repressor from the OCT4 promoter was considered to account for valproic acid-induced up-regulation of OCT4 expression in mouse myoblast C2C12 cells and mouse embryonic carcinoma P19 cells33, and knocking-down OCT4 in pancreatic cancer cells decreased the mRNA and protein levels of total AKT34, implicating a positive correlation between AKT and OCT4. This evidence concerns the gene AKT1 and embryonal carcinoma.