Overall, despite different degrees of involvement and underlying mechanisms, loss of cadherins (E-cadherin and N-cadherin) or catenins (p120-and α-catenin) results in NF-κB hyperactivation and production of pro-inflammatory signals that globally regulate the TME, induce immune infiltration and desmoplasia, and promote tumor progression. The gene discussed is CTNND1; the disease is neoplasm.