Lastly, given that PrE-like differentiation in F9 teratocarcinoma cells was shown to require p38-Mapk14/11 mediated inhibition of Gsk3β function [35], we tested if our observed uncommitted ICM phenotype could be rescued by direct pharmacological inhibition of Gsk3β itself and found that it could not. This evidence concerns the gene MAPK14 and teratocarcinoma.