A dependency of ARID1A-mutated tumors on activation of the PI3K/AKT pathway is further supported by a study in ARID1A-knockout and ARID1A/PTEN-double-knockout mice, where it was observed that only mice with simultaneous loss of ARID1A and PTEN expression developed poorly differentiated ovarian tumors, in contrast to mice with loss of only ARID1A that did not develop ovarian tumors [29]. Here, AKT1 is linked to ovarian neoplasm.