However, previous studies probing into the mechanism of PRL-3 in other cancers demonstrated that the phosphatase downregulated the expression of another phosphatase known as phosphatase and tensin homologue (PTEN), leading to the upregulation of the PI3K-AKT pathway through signaling modalities that were previously described (Figure 2A) [64,65]. The gene discussed is PTEN; the disease is cancer.