AKT1 and ovarian carcinoma: For example, induction of p53 and transfection of ERK activating RAS mutants but not AKT activating RAS mutant in p53-null ovarian cancer cells promoted autophagy, although the autophagy induced by p53 or ERK activating RAS mutants showed an opposite sensitivity to cisplatin treatment because the activation of RAS/ERK ultimately lead to the increased expression of p-ERK and Bcl-2 and the decreased expression of p-AKT and Bax [101].