BAY1082439′s anti-PI3Kα/β activities not only inhibit PTEN null prostate cancer cells growth and prevent feedback activation between PI3K isoforms51, but can revert PI3K-dependent immunosuppressive activity by upregulating IFN signaling pathway activity, CXCL10 and CCL5 excretion and B2M expression. This evidence concerns the gene PTEN and prostate carcinoma.