GluIIβ was reported to be frequently overexpressed in non-small cell lung carcinoma (NSCLC)3 and suppression of its expression and/or activity has been reported to dose dependently inactivated EGFR/RTK and PI3K/AKT signaling pathways4, causing autophagy4,5 and apoptosis4,6. Here, AKT1 is linked to non-small cell lung carcinoma.