In addition, MAGI-2 is found in tumor studies to interact with PTEN via its PDZ2 domain and thereby stabilizes the structure of PTEN, increases its membrane trafficking, and enhances its inhibitory effect on Akt signaling and tumor pathogenesis (Wu et al., 2000; Tolkacheva et al., 2001; Nagashima et al., 2015). The gene discussed is AKT1; the disease is neoplasm.