AP-1 is under the direct regulatory control of MAP kinases, which phosphorylate the Jun and Fos components of AP-1 protein and facilitate their target binding [46], [54].The presence of high concentrations of bile acids also induces the AP-1 expression in colon cells via PKC and ERK1/2 signaling, resulting in tumor promotion [55].Treatment with PMA activates both NF-kappaB and AP-1 transcription factors through Ras/Raf/ERK1/2, JNK and phosphoinositise-3-kinase/Akt signaling pathways [56], [57]. The gene discussed is AKT1; the disease is neoplasm.