Although the mechanism is unknown, phosphorylation of PI3K downstream targets, including PDK1, AKT, TSC2 and S6K, was significantly upregulated in the presence of ARID1A mutations, and knockdown of wild-type ARID1A in three endometrial cancer cell lines resulted in significantly elevated phosphorylation of AKT [32]. The gene discussed is AKT1; the disease is endometrial cancer.