MAPK3 and colon carcinoma: Fig 3 shows the increase in phosphorylation that was observed for Erk1/2 as a result of treatment with UDCA. Erk1/2 activation-induced arrest of cell cycle progression in colon carcinoma and colonic epithelial cells is well known [26, 32, 33]. p38 kinase is also known to contribute to cellular proliferation and stress response. Fig 3 shows that inactivation of p38 kinase by UDCA suppressed proliferation.