MAPK8 and neoplasm: Mechanistic studies of DGC revealed that the inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)—a potent tumor promoter [109,110]—induced phosphorylation of p38 MAPK, JNK and Akt, a major substrate of phosphoinositide 3-kinase (PI3K) [111].