Notably, Inpp4B loss and Pten heterozygous deletion can cooperate in mice to facilitate metastatic thyroid cancer by increasing PIP3 levels and AKT signaling relative to single mutants [115], and enforced INPP4B overexpression in PC3 (PTEN−/−) and DU145 (PTEN+/−) prostate cancer cells can suppress prostate cancer cell migration and invasion, both in vitro and in vivo [117]. The gene discussed is PTEN; the disease is prostate carcinoma.