Since the activation of AKT and ERK contributes to cell survival and growth, we further assayed and verified marked inhibitions in the levels of both p-AKT and p-ERK (Fig. 4b), indicating that transient overexpression of TIPE3 with N-terminal flag by plasmid transfection led to the cytoplasmic localization of exogenous TIPE3, which inhibited the proliferation and migration of lung cancer cells by inactivating AKT and ERK. The gene discussed is AKT1; the disease is lung carcinoma.