Overexpression of the PTENP1 3’-UTR led to increased levels of PTENP1, thereby isolating miRNAs and countering the PI3K/AKT pathway, reducing cell proliferation and metastatic tumors and increasing programmed cell death in the prostate (DU145) [28], kidney (ACHN and SN12MP6) [112], liver (SK-Hep1 and SMMC-7721) [114], and breast (MCF-7 and MDA-MB-231) [115, 116], bladder (T24 and T5637) [117], gastric (MGC803 and BGC823) [33], esophageal (Eca19), cervical (CasKi and HeLa) [118], and endometrial (RL-952, JEC, and HEC-1B) cancer cell lines [62]. The gene discussed is AKT1; the disease is metastatic neoplasm.