Recently, Yan and colleagues (42) also reported that CNTN1 overexpression induced elevated AKT activation and reduced E-cadherin (CDH1) in DU145 cells and corresponding xenograft tumors and that knockdown of CNTN1 reduced tumor initiation mediated by PCa stem-like cells, which is consistent with the results in our presented research. The gene discussed is AKT1; the disease is posterior cortical atrophy.