Taken together, these results (Figs 4 and 5) suggest that AKT1-MARCKS-LAMC2 forms a feedback regulation loop in the KRAS or EGFR mutant NSCLC cells: AKT1 inhibition induces MARCKS phosphorylation, leading to upregulation of LAMC2 expression to promote cell migration and invasion, whereas increased LAMC2 inhibits AKT1 signaling, thus amplifying the effect of AKT1 inhibition on these cellular processes. Here, MARCKS is linked to non-small cell lung carcinoma.