By differential analysis, we found that the subset of tested cancer cell lines that responded to BET inhibition with GDF15 reduction and GDF11 induction show a higher activity of p38 MAPK and a significantly lower activity of and dependency on proteins involved in the PI3K/Akt pathway, namely GSK3B, Akt, Bcl and B-Raf, compared to the weakly responding cell lines. Here, AKT1 is linked to cancer.