MARK2 and carcinoma: In p53-deficient cells, α6β4-integrins promoted AKT-dependent survival of carcinoma cells, whereas in carcinomas expressing functional p53, α6β4-integrins stimulated the cleavage and inactivation of serine/threonine kinase AKT in caspase-3-dependent manner, indicating that p53 can inhibit survival signals emanating from α6β4-integrins [123].