The TMED3-mediated activation of Wnt/β-catenin signaling is further validated by Zhang D and collaborators, who demonstrate that in NSCLC, TMED3 stimulates the activation of AKT, which, in turn, phosphorylates GSK3β at Ser9, causing GSK3β inactivation, which, in turn, leads to β-catenin activation, thus resulting in increased expression of N-cadherin and vimentin, decreased expression of E-cadherin, and, consequently, increased invasion of NSCLC cells [56]. Here, AKT1 is linked to non-small cell lung carcinoma.