AKT1 and glioblastoma: The C-E-Cad 14-aa tail enables direct binding to the CR2 domain of full-length EGFR through salt bridge and hydrogen bond interactions, accompanied by EGFRvIII to promote STAT3 phosphorylation and nuclear translocation and AKT and ERK1/2 phosphorylation, resulting in the tumorigenicity of GBM [46, 105].