Loss-of-function mutations in ARID1A often co-occur with activating mutations in PI3K, AKT or mTOR or with loss of PTEN, which all result in upregulation of PI3K/AKT signaling, However, the finding that the small-molecule SMARCA4/2 inhibitor PFI-3 has a promising therapeutic activity in preclinical models of PTEN-deficient prostate cancer suggests additional complexity in the relationship between the PI3K/AKT axis and SWI/SNF function [47]. The gene discussed is ARID1A; the disease is Familial prostate cancer.